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Tytuł pozycji:

Interplay between inflammation and thrombosis in cardiovascular pathology.

Tytuł:
Interplay between inflammation and thrombosis in cardiovascular pathology.
Autorzy:
Stark K; Medizinische Klinik und Poliklinik I, University Hospital, LMU Munich, Munich, Germany. .; German Center for Cardiovascular Research (DZHK), partner site Munich Heart Alliance, Munich, Germany. .; Walter-Brendel Center of Experimental Medicine, Faculty of Medicine, LMU Munich, Munich, Germany. .
Massberg S; Medizinische Klinik und Poliklinik I, University Hospital, LMU Munich, Munich, Germany. .; German Center for Cardiovascular Research (DZHK), partner site Munich Heart Alliance, Munich, Germany. .; Walter-Brendel Center of Experimental Medicine, Faculty of Medicine, LMU Munich, Munich, Germany. .
Źródło:
Nature reviews. Cardiology [Nat Rev Cardiol] 2021 Sep; Vol. 18 (9), pp. 666-682. Date of Electronic Publication: 2021 May 06.
Typ publikacji:
Journal Article; Review
Język:
English
Imprint Name(s):
Original Publication: London : Nature Pub. Group
MeSH Terms:
Anti-Inflammatory Agents/*therapeutic use
Blood Coagulation/*drug effects
Fibrinolytic Agents/*therapeutic use
Immune System/*drug effects
Inflammation/*drug therapy
Inflammation Mediators/*antagonists & inhibitors
Thrombosis/*prevention & control
Anti-Inflammatory Agents/adverse effects ; COVID-19/blood ; COVID-19/immunology ; Fibrinolytic Agents/adverse effects ; Humans ; Immune System/immunology ; Immune System/metabolism ; Inflammation/blood ; Inflammation/immunology ; Inflammation Mediators/metabolism ; Risk Assessment ; Risk Factors ; Signal Transduction ; Thrombosis/blood ; Thrombosis/immunology
References:
Engelmann, B. & Massberg, S. Thrombosis as an intravascular effector of innate immunity. Nat. Rev. Immunol. 13, 34–45 (2013). (PMID: 2322250210.1038/nri3345)
Ackermann, M. et al. Pulmonary vascular endothelialitis, thrombosis, and angiogenesis in Covid-19. N. Engl. J. Med. 383, 120–128 (2020). (PMID: 32437596741275010.1056/NEJMoa2015432)
Nicolai, L. et al. Immunothrombotic dysregulation in COVID-19 pneumonia is associated with respiratory failure and coagulopathy. Circulation 142, 1176–1189 (2020). (PMID: 32755393749789210.1161/CIRCULATIONAHA.120.048488)
Wichmann, D. et al. Autopsy findings and venous thromboembolism in patients with COVID-19: a prospective cohort study. Ann. Intern. Med. 173, 268–277 (2020). (PMID: 3237481510.7326/M20-2003)
Creel-Bulos, C. et al. Acute cor pulmonale in critically ill patients with Covid-19. N. Engl. J. Med. 382, e70 (2020). (PMID: 3237495610.1056/NEJMc2010459)
Cui, S., Chen, S., Li, X., Liu, S. & Wang, F. Prevalence of venous thromboembolism in patients with severe novel coronavirus pneumonia. J. Thromb. Haemost. 18, 1421–1424 (2020). (PMID: 3227198810.1111/jth.14830)
Klok, F. A. et al. Confirmation of the high cumulative incidence of thrombotic complications in critically ill ICU patients with COVID-19: An updated analysis. Thromb. Res. 191, 148–150 (2020). (PMID: 32381264719210110.1016/j.thromres.2020.04.041)
Klok, F. A. et al. Incidence of thrombotic complications in critically ill ICU patients with COVID-19. Thromb. Res. 191, 145–147 (2020). (PMID: 32291094714671410.1016/j.thromres.2020.04.013)
Poissy, J. et al. Pulmonary embolism in COVID-19 patients: awareness of an increased prevalence. Circulation 142, 184–186 (2020). (PMID: 3233008310.1161/CIRCULATIONAHA.120.047430)
Oxley, T. J. et al. Large-vessel stroke as a presenting feature of Covid-19 in the young. N. Engl. J. Med. 382, e60 (2020). (PMID: 3234350410.1056/NEJMc2009787)
Bangalore, S. et al. ST-segment elevation in patients with Covid-19 – a case series. N. Engl. J. Med. 382, 2478–2480 (2020). (PMID: 3230208110.1056/NEJMc2009020)
Stefanini, G. G. et al. ST-elevation myocardial infarction in patients with COVID-19: clinical and angiographic outcomes. Circulation 141, 2113–2116 (2020). (PMID: 32352306730206210.1161/CIRCULATIONAHA.120.047525)
Jackson, S. P. Arterial thrombosis–insidious, unpredictable and deadly. Nat. Med. 17, 1423–1436 (2011). (PMID: 2206443210.1038/nm.2515)
Mackman, N. Triggers, targets and treatments for thrombosis. Nature 451, 914–918 (2008). (PMID: 18288180284850910.1038/nature06797)
Mackman, N. New insights into the mechanisms of venous thrombosis. J. Clin. Invest. 122, 2331–2336 (2012). (PMID: 22751108338681110.1172/JCI60229)
Hottz, E. D. et al. Platelets mediate increased endothelium permeability in dengue through NLRP3-inflammasome activation. Blood 122, 3405–3414 (2013). (PMID: 24009231382911410.1182/blood-2013-05-504449)
Semple, J. W., Italiano, J. E. Jr. & Freedman, J. Platelets and the immune continuum. Nat. Rev. Immunol. 11, 264–274 (2011). (PMID: 2143683710.1038/nri2956)
Gaertner, F. et al. Migrating platelets are mechano-scavengers that collect and bundle bacteria. Cell 171, 1368–1382 (2017). (PMID: 2919507610.1016/j.cell.2017.11.001)
Nicolai, L. et al. Vascular surveillance by haptotactic blood platelets in inflammation and infection. Nat. Commun. 11, 5778 (2020). (PMID: 33188196766658210.1038/s41467-020-19515-0)
Brinkmann, V. et al. Neutrophil extracellular traps kill bacteria. Science 303, 1532–1535 (2004). (PMID: 10.1126/science.109238515001782)
Fuchs, T. A. et al. Extracellular DNA traps promote thrombosis. Proc. Natl Acad. Sci. USA 107, 15880–15885 (2010). (PMID: 20798043293660410.1073/pnas.1005743107)
von Bruhl, M. L. et al. Monocytes, neutrophils, and platelets cooperate to initiate and propagate venous thrombosis in mice in vivo. J. Exp. Med. 209, 819–835 (2012). (PMID: 10.1084/jem.20112322)
Xu, J. et al. Extracellular histones are major mediators of death in sepsis. Nat. Med. 15, 1318–1321 (2009). (PMID: 19855397278375410.1038/nm.2053)
Kenny, E. F. et al. Diverse stimuli engage different neutrophil extracellular trap pathways. eLife 6, e24437 (2017). (PMID: 28574339549673810.7554/eLife.24437)
Lewis, H. D. et al. Inhibition of PAD4 activity is sufficient to disrupt mouse and human NET formation. Nat. Chem. Biol. 11, 189–191 (2015). (PMID: 25622091439758110.1038/nchembio.1735)
Martinod, K. et al. Neutrophil histone modification by peptidylarginine deiminase 4 is critical for deep vein thrombosis in mice. Proc. Natl Acad. Sci. USA 110, 8674–8679 (2013). (PMID: 23650392366675510.1073/pnas.1301059110)
Li, P. et al. PAD4 is essential for antibacterial innate immunity mediated by neutrophil extracellular traps. J. Exp. Med. 207, 1853–1862 (2010). (PMID: 20733033293116910.1084/jem.20100239)
Sollberger, G., Tilley, D. O. & Zychlinsky, A. Neutrophil extracellular traps: the biology of chromatin externalization. Dev. Cell 44, 542–553 (2018). (PMID: 2953377010.1016/j.devcel.2018.01.019)
Silvestre-Roig, C., Hidalgo, A. & Soehnlein, O. Neutrophil heterogeneity: implications for homeostasis and pathogenesis. Blood 127, 2173–2181 (2016). (PMID: 2700211610.1182/blood-2016-01-688887)
Uhl, B. et al. Aged neutrophils contribute to the first line of defense in the acute inflammatory response. Blood 128, 2327–2337 (2016). (PMID: 27609642512231010.1182/blood-2016-05-718999)
Zhang, D. et al. Neutrophil ageing is regulated by the microbiome. Nature 525, 528–532 (2015). (PMID: 26374999471263110.1038/nature15367)
Jimenez-Alcazar, M. et al. Host DNases prevent vascular occlusion by neutrophil extracellular traps. Science 358, 1202–1206 (2017). (PMID: 2919191010.1126/science.aam8897)
Hakkim, A. et al. Impairment of neutrophil extracellular trap degradation is associated with lupus nephritis. Proc. Natl Acad. Sci. USA 107, 9813–9818 (2010). (PMID: 20439745290683010.1073/pnas.0909927107)
Sreeramkumar, V. et al. Neutrophils scan for activated platelets to initiate inflammation. Science 346, 1234–1238 (2014). (PMID: 25477463428084710.1126/science.1256478)
Clark, S. R. et al. Platelet TLR4 activates neutrophil extracellular traps to ensnare bacteria in septic blood. Nat. Med. 13, 463–469 (2007). (PMID: 1738464810.1038/nm1565)
Rossaint, J. et al. Directed transport of neutrophil-derived extracellular vesicles enables platelet-mediated innate immune response. Nat. Commun. 7, 13464 (2016). (PMID: 27845343511607210.1038/ncomms13464)
Verschoor, A. & Langer, H. F. Crosstalk between platelets and the complement system in immune protection and disease. Thromb. Haemost. 110, 910–919 (2013). (PMID: 2400892710.1160/TH13-02-0102)
Schmidt, C. Q. & Verschoor, A. Complement and coagulation: so close, yet so far. Blood 130, 2581–2582 (2017). (PMID: 2924220710.1182/blood-2017-10-811943)
Peerschke, E. I., Yin, W. & Ghebrehiwet, B. Complement activation on platelets: implications for vascular inflammation and thrombosis. Mol. Immunol. 47, 2170–2175 (2010). (PMID: 20621693290432610.1016/j.molimm.2010.05.009)
Polley, M. J. & Nachman, R. The human complement system in thrombin-mediated platelet function. J. Exp. Med. 147, 1713–1726 (1978). (PMID: 68187910.1084/jem.147.6.1713)
Verschoor, A. et al. A platelet-mediated system for shuttling blood-borne bacteria to CD8α dendritic cells depends on glycoprotein GPIb and complement C3. Nat. Immunol. 12, 1194–1201 (2011). (PMID: 2203760210.1038/ni.2140)
Massberg, S. et al. Reciprocal coupling of coagulation and innate immunity via neutrophil serine proteases. Nat. Med. 16, 887–896 (2010). (PMID: 2067610710.1038/nm.2184)
Yipp, B. G. et al. Infection-induced NETosis is a dynamic process involving neutrophil multitasking in vivo. Nat. Med. 18, 1386–1393 (2012). (PMID: 22922410452913110.1038/nm.2847)
Wu, C. et al. Inflammasome activation triggers blood clotting and host death through pyroptosis. Immunity 50, 1401–1411 (2019). (PMID: 31076358679153110.1016/j.immuni.2019.04.003)
Bach, R., Gentry, R. & Nemerson, Y. Factor VII binding to tissue factor in reconstituted phospholipid vesicles: induction of cooperativity by phosphatidylserine. Biochemistry 25, 4007–4020 (1986). (PMID: 352726110.1021/bi00362a005)
Yang, X. et al. Bacterial endotoxin activates the coagulation cascade through gasdermin D-dependent phosphatidylserine exposure. Immunity 51, 983–996 (2019). (PMID: 3183642910.1016/j.immuni.2019.11.005)
Reinhardt, C. et al. Protein disulfide isomerase acts as an injury response signal that enhances fibrin generation via tissue factor activation. J. Clin. Invest. 118, 1110–1122 (2008). (PMID: 182746742242616)
Burzynski, L. C. et al. The coagulation and immune systems are directly linked through the activation of interleukin-1α by thrombin. Immunity 50, 1033–1042 (2019). (PMID: 30926232647640410.1016/j.immuni.2019.03.003)
Pietras, E. M. Inflammation: a key regulator of hematopoietic stem cell fate in health and disease. Blood 130, 1693–1698 (2017). (PMID: 28874349563948510.1182/blood-2017-06-780882)
Haas, S. et al. Inflammation-induced emergency megakaryopoiesis driven by hematopoietic stem cell-like megakaryocyte progenitors. Cell Stem Cell 17, 422–434 (2015). (PMID: 2629957310.1016/j.stem.2015.07.007)
Schönrich, G. & Raftery, M. J. Neutrophil extracellular traps go viral. Front. Immunol. 7, 366 (2016). (PMID: 27698656502720510.3389/fimmu.2016.00366)
Jenne, C. N. et al. Neutrophils recruited to sites of infection protect from virus challenge by releasing neutrophil extracellular traps. Cell Host Microbe 13, 169–180 (2013). (PMID: 2341475710.1016/j.chom.2013.01.005)
Boilard, E. et al. Influenza virus H1N1 activates platelets through FcγRIIA signaling and thrombin generation. Blood 123, 2854–2863 (2014). (PMID: 2466513610.1182/blood-2013-07-515536)
Koupenova, M. et al. The role of platelets in mediating a response to human influenza infection. Nat. Commun. 10, 1780 (2019). (PMID: 30992428646790510.1038/s41467-019-09607-x)
Funchal, G. A. et al. Respiratory syncytial virus fusion protein promotes TLR-4-dependent neutrophil extracellular trap formation by human neutrophils. PLoS ONE 10, e0124082 (2015). (PMID: 25856628439175010.1371/journal.pone.0124082)
Tripathi, S., Verma, A., Kim, E. J., White, M. R. & Hartshorn, K. L. LL-37 modulates human neutrophil responses to influenza A virus. J. Leukoc. Biol. 96, 931–938 (2014). (PMID: 25082153419756310.1189/jlb.4A1113-604RR)
Narasaraju, T. et al. Excessive neutrophils and neutrophil extracellular traps contribute to acute lung injury of influenza pneumonitis. Am. J. Pathol. 179, 199–210 (2011). (PMID: 21703402312387310.1016/j.ajpath.2011.03.013)
Nicolai, L. et al. Vascular neutrophilic inflammation and immunothrombosis distinguish severe COVID-19 from influenza pneumonia. J. Thromb. Haemost. 19, 574–581 (2020). (PMID: 3321713410.1111/jth.15179)
Doss, M. et al. Interactions of α-, β-, and θ-defensins with influenza A virus and surfactant protein D. J. Immunol. 182, 7878–7887 (2009). (PMID: 1949431210.4049/jimmunol.0804049)
Hartshorn, K. L., White, M. R., Tecle, T., Holmskov, U. & Crouch, E. C. Innate defense against influenza A virus: activity of human neutrophil defensins and interactions of defensins with surfactant protein D. J. Immunol. 176, 6962–6972 (2006). (PMID: 1670985710.4049/jimmunol.176.11.6962)
Salvatore, M. et al. α-Defensin inhibits influenza virus replication by cell-mediated mechanism(s). J. Infect. Dis. 196, 835–843 (2007). (PMID: 1770341310.1086/521027)
Barlow, P. G. et al. Antiviral activity and increased host defense against influenza infection elicited by the human cathelicidin LL-37. PLoS ONE 6, e25333 (2011). (PMID: 22031815319873410.1371/journal.pone.0025333)
Meier, C. R., Jick, S. S., Derby, L. E., Vasilakis, C. & Jick, H. Acute respiratory-tract infections and risk of first-time acute myocardial infarction. Lancet 351, 1467–1471 (1998). (PMID: 960580210.1016/S0140-6736(97)11084-4)
Smeeth, L. et al. Risk of myocardial infarction and stroke after acute infection or vaccination. N. Engl. J. Med. 351, 2611–2618 (2004). (PMID: 1560202110.1056/NEJMoa041747)
Corrales-Medina, V. F. et al. Cardiac complications in patients with community-acquired pneumonia: incidence, timing, risk factors, and association with short-term mortality. Circulation 125, 773–781 (2012). (PMID: 2221934910.1161/CIRCULATIONAHA.111.040766)
Dalager-Pedersen, M., Sogaard, M., Schonheyder, H. C., Nielsen, H. & Thomsen, R. W. Risk for myocardial infarction and stroke after community-acquired bacteremia: a 20-year population-based cohort study. Circulation 129, 1387–1396 (2014). (PMID: 2452343310.1161/CIRCULATIONAHA.113.006699)
Beristain-Covarrubias, N. et al. Understanding infection-induced thrombosis: lessons learned from animal models. Front. Immunol. 10, 2569 (2019). (PMID: 31749809684806210.3389/fimmu.2019.02569)
Grayston, J. T. et al. Azithromycin for the secondary prevention of coronary events. N. Engl. J. Med. 352, 1637–1645 (2005). (PMID: 1584366610.1056/NEJMoa043526)
O’Connor, C. M. et al. Azithromycin for the secondary prevention of coronary heart disease events: the WIZARD study: a randomized controlled trial. JAMA 290, 1459–1466 (2003). (PMID: 1312998510.1001/jama.290.11.1459)
McDonald, B. et al. Platelets and neutrophil extracellular traps collaborate to promote intravascular coagulation during sepsis in mice. Blood 129, 1357–1367 (2017). (PMID: 28073784534573510.1182/blood-2016-09-741298)
Schumski, A. et al. Endotoxinemia accelerates atherosclerosis via electrostatic charge-mediated monocyte adhesion. Circulation 143, 254–266 (2020). (PMID: 3316768410.1161/CIRCULATIONAHA.120.0466777914394)
Ammollo, C. T., Semeraro, F., Xu, J., Esmon, N. L. & Esmon, C. T. Extracellular histones increase plasma thrombin generation by impairing thrombomodulin-dependent protein C activation. J. Thromb. Haemost. 9, 1795–1803 (2011). (PMID: 2171144410.1111/j.1538-7836.2011.04422.x)
Semeraro, F., Ammollo, C. T., Esmon, N. L. & Esmon, C. T. Histones induce phosphatidylserine exposure and a procoagulant phenotype in human red blood cells. J. Thromb. Haemost. 12, 1697–1702 (2014). (PMID: 25069624419415410.1111/jth.12677)
Semeraro, F. et al. Extracellular histones promote thrombin generation through platelet-dependent mechanisms: involvement of platelet TLR2 and TLR4. Blood 118, 1952–1961 (2011). (PMID: 21673343315872210.1182/blood-2011-03-343061)
Landsem, A. et al. The key roles of complement and tissue factor in Escherichia coli-induced coagulation in human whole blood. Clin. Exp. Immunol. 182, 81–89 (2015). (PMID: 26241501457851110.1111/cei.12663)
Ovstebo, R. et al. Microparticle-associated tissue factor activity is reduced by inhibition of the complement protein 5 in Neisseria meningitidis-exposed whole blood. Innate Immun. 20, 552–560 (2014). (PMID: 2405110210.1177/1753425913502099)
Norgaard, I., Nielsen, S. F. & Nordestgaard, B. G. Complement C3 and high risk of venous thromboembolism: 80517 individuals from the Copenhagen general population study. Clin. Chem. 62, 525–534 (2016). (PMID: 2679768610.1373/clinchem.2015.251314)
Goshua, G. et al. Endotheliopathy in COVID-19-associated coagulopathy: evidence from a single-centre, cross-sectional study. Lancet Haematol. 7, e575–e582 (2020). (PMID: 32619411732644610.1016/S2352-3026(20)30216-7)
Zhang, Y. et al. Coagulopathy and antiphospholipid antibodies in patients with Covid-19. N. Engl. J. Med. 382, e38 (2020). (PMID: 3226802210.1056/NEJMc2007575)
Zhou, F. et al. Clinical course and risk factors for mortality of adult inpatients with COVID-19 in Wuhan, China: a retrospective cohort study. Lancet 395, 1054–1062 (2020). (PMID: 32171076727062710.1016/S0140-6736(20)30566-3)
Tang, N., Li, D., Wang, X. & Sun, Z. Abnormal coagulation parameters are associated with poor prognosis in patients with novel coronavirus pneumonia. J. Thromb. Haemost. 18, 844–847 (2020). (PMID: 32073213716650910.1111/jth.14768)
Chen, G. et al. Clinical and immunological features of severe and moderate coronavirus disease 2019. J. Clin. Invest. 130, 2620–2629 (2020). (PMID: 32217835719099010.1172/JCI137244)
Hamming, I. et al. Tissue distribution of ACE2 protein, the functional receptor for SARS coronavirus. A first step in understanding SARS pathogenesis. J. Pathol. 203, 631–637 (2004). (PMID: 15141377716772010.1002/path.1570)
Varga, Z. et al. Endothelial cell infection and endotheliitis in COVID-19. Lancet 395, 1417–1418 (2020). (PMID: 32325026717272210.1016/S0140-6736(20)30937-5)
Mancini, I. et al. The ADAMTS13-von Willebrand factor axis in COVID-19 patients. J. Thromb. Haemost. 19, 513–521 (2020). (PMID: 3323090410.1111/jth.15191)
Aid, M. et al. Vascular disease and thrombosis in SARS-CoV-2-infected rhesus macaques. Cell 183, 1354–1366 (2020). (PMID: 33065030754618110.1016/j.cell.2020.10.005)
Bazzan, M. et al. Low ADAMTS 13 plasma levels are predictors of mortality in COVID-19 patients. Intern. Emerg. Med. 15, 861–863 (2020). (PMID: 3255738310.1007/s11739-020-02394-07300200)
Zuo, Y. et al. Prothrombotic autoantibodies in serum from patients hospitalized with COVID-19. Sci. Transl Med. 12, eabd3876 (2020). (PMID: 33139519772427310.1126/scitranslmed.abd3876)
Manne, B. K. et al. Platelet gene expression and function in COVID-19 patients. Blood 136, 1317–1329 (2020). (PMID: 3257371110.1182/blood.2020007214)
Everitt, A. R. et al. IFITM3 restricts the morbidity and mortality associated with influenza. Nature 484, 519–523 (2012). (PMID: 22446628364878610.1038/nature10921)
Zhang, Y. et al. Interferon-induced transmembrane protein 3 genetic variant rs12252-C associated with disease severity in coronavirus disease 2019. J. Infect. Dis. 222, 34–37 (2020). (PMID: 32348495719755910.1093/infdis/jiaa224)
Bernardes, J. P. et al. Longitudinal multi-omics analyses identify responses of megakaryocytes, erythroid cells, and plasmablasts as hallmarks of severe COVID-19. Immunity 53, 1296–1314 (2020). (PMID: 33296687768930610.1016/j.immuni.2020.11.017)
Campbell, R. A. et al. Human megakaryocytes possess intrinsic antiviral immunity through regulated induction of IFITM3. Blood 133, 2013–2026 (2019). (PMID: 30723081650954610.1182/blood-2018-09-873984)
Zuo, Y. et al. Neutrophil extracellular traps in COVID-19. JCI Insight 5, e138999 (2020). (PMID: 7308057)
Middleton, E. A. et al. Neutrophil extracellular traps (NETs) contribute to immunothrombosis in COVID-19 acute respiratory distress syndrome. Blood 136, 1169–1179 (2020). (PMID: 3259795410.1182/blood.2020007008)
Rossaint, J. et al. Synchronized integrin engagement and chemokine activation is crucial in neutrophil extracellular trap-mediated sterile inflammation. Blood 123, 2573–2584 (2014). (PMID: 2433523010.1182/blood-2013-07-516484)
Yost, C. C. et al. Neonatal NET-inhibitory factor and related peptides inhibit neutrophil extracellular trap formation. J. Clin. Invest. 126, 3783–3798 (2016). (PMID: 27599294509680910.1172/JCI83873)
Veras, F. P. et al. SARS-CoV-2-triggered neutrophil extracellular traps mediate COVID-19 pathology. J. Exp. Med. 217, e20201129 (2020). (PMID: 32926098748886810.1084/jem.20201129)
Blasco, A. et al. Assessment of neutrophil extracellular traps in coronary thrombus of a case series of patients with COVID-19 and myocardial infarction. JAMA Cardiol. 6, 469–474 (2021). (PMID: 10.1001/jamacardio.2020.7308)
Hottz, E. D. et al. Platelet activation and platelet-monocyte aggregate formation trigger tissue factor expression in patients with severe COVID-19. Blood 136, 1330–1341 (2020). (PMID: 3267842810.1182/blood.2020007252)
Ramlall, V. et al. Immune complement and coagulation dysfunction in adverse outcomes of SARS-CoV-2 infection. Nat. Med. 26, 1609–1615 (2020). (PMID: 32747830780963410.1038/s41591-020-1021-2)
Magro, C. et al. Complement associated microvascular injury and thrombosis in the pathogenesis of severe COVID-19 infection: a report of five cases. Transl Res. 220, 1–13 (2020). (PMID: 32299776715824810.1016/j.trsl.2020.04.007)
Skendros, P. et al. Complement and tissue factor-enriched neutrophil extracellular traps are key drivers in COVID-19 immunothrombosis. J. Clin. Invest. 130, 6151–6157 (2020). (PMID: 32759504759804010.1172/JCI141374)
Gralinski, L. E. et al. Complement activation contributes to severe acute respiratory syndrome coronavirus pathogenesis. mBio 9, e01753-18 (2018). (PMID: 30301856617862110.1128/mBio.01753-18)
Jiang, Y. et al. Blockade of the C5a-C5aR axis alleviates lung damage in hDPP4-transgenic mice infected with MERS-CoV. Emerg. Microbes Infect. 7, 77 (2018). (PMID: 29691378591558010.1038/s41426-018-0063-8)
Le, V. B. et al. Platelet activation and aggregation promote lung inflammation and influenza virus pathogenesis. Am. J. Respir. Crit. Care Med. 191, 804–819 (2015). (PMID: 2566439110.1164/rccm.201406-1031OC)
Risitano, A. M. et al. Complement as a target in COVID-19? Nat. Rev. Immunol. 20, 343–344 (2020). (PMID: 3232771910.1038/s41577-020-0320-7)
Duerschmied, D. et al. Platelet serotonin promotes the recruitment of neutrophils to sites of acute inflammation in mice. Blood 121, 1008–1015 (2013). (PMID: 23243271356733510.1182/blood-2012-06-437392)
Karshovska, E., Weber, C. & von Hundelshausen, P. Platelet chemokines in health and disease. Thromb. Haemost. 110, 894–902 (2013). (PMID: 2378340110.1160/TH13-04-0341)
Palabrica, T. et al. Leukocyte accumulation promoting fibrin deposition is mediated in vivo by P-selectin on adherent platelets. Nature 359, 848–851 (1992). (PMID: 127943310.1038/359848a0)
Wang, Y. et al. Leukocyte integrin Mac-1 regulates thrombosis via interaction with platelet GPIbα. Nat. Commun. 8, 15559 (2017). (PMID: 28555620547751910.1038/ncomms15559)
Downing, L. J. et al. Anti-P-selectin antibody decreases inflammation and thrombus formation in venous thrombosis. J. Vasc. Surg. 25, 816–827 (1997). (PMID: 915230910.1016/S0741-5214(97)70211-8)
Myers, D. D. Jr. et al. Decreased venous thrombosis with an oral inhibitor of P selectin. J. Vasc. Surg. 42, 329–336 (2005). (PMID: 1610263510.1016/j.jvs.2005.04.045)
Blann, A. D., Nadar, S. K. & Lip, G. Y. The adhesion molecule P-selectin and cardiovascular disease. Eur. Heart J. 24, 2166–2179 (2003). (PMID: 1465976810.1016/j.ehj.2003.08.021)
Ridker, P. M., Buring, J. E. & Rifai, N. Soluble P-selectin and the risk of future cardiovascular events. Circulation 103, 491–495 (2001). (PMID: 1115771110.1161/01.CIR.103.4.491)
Riegger, J. et al. Histopathological evaluation of thrombus in patients presenting with stent thrombosis. A multicenter European study: a report of the prevention of late stent thrombosis by an interdisciplinary global European effort consortium. Eur. Heart J. 37, 1538–1549 (2016). (PMID: 2676195010.1093/eurheartj/ehv419)
Savchenko, A. S. et al. Neutrophil extracellular traps form predominantly during the organizing stage of human venous thromboembolism development. J. Thromb. Haemost. 12, 860–870 (2014). (PMID: 24674135405551610.1111/jth.12571)
Etulain, J. et al. P-selectin promotes neutrophil extracellular trap formation in mice. Blood 126, 242–246 (2015). (PMID: 25979951449796410.1182/blood-2015-01-624023)
Maugeri, N. et al. Activated platelets present high mobility group Box 1 to neutrophils, inducing autophagy and promoting the extrusion of neutrophil extracellular traps. J. Thromb. Haemost. 12, 2074–2088 (2014). (PMID: 2516351210.1111/jth.12710)
Stark, K. et al. Disulfide HMGB1 derived from platelets coordinates venous thrombosis in mice. Blood 128, 2435–2449 (2016). (PMID: 27574188514702310.1182/blood-2016-04-710632)
Noubouossie, D. F., Reeves, B. N., Strahl, B. D. & Key, N. S. Neutrophils: back in the thrombosis spotlight. Blood 133, 2186–2197 (2019). (PMID: 30898858721873110.1182/blood-2018-10-862243)
Noubouossie, D. F. et al. In vitro activation of coagulation by human neutrophil DNA and histone proteins but not neutrophil extracellular traps. Blood 129, 1021–1029 (2017). (PMID: 27919911532471510.1182/blood-2016-06-722298)
Pircher, J. et al. Cathelicidins prime platelets to mediate arterial thrombosis and tissue inflammation. Nat. Commun. 9, 1523 (2018). (PMID: 29670076590663610.1038/s41467-018-03925-2)
Doring, Y. et al. Lack of neutrophil-derived CRAMP reduces atherosclerosis in mice. Circ. Res. 110, 1052–1056 (2012). (PMID: 2239451910.1161/CIRCRESAHA.112.265868)
Soehnlein, O. et al. Neutrophil-derived cathelicidin protects from neointimal hyperplasia. Sci. Transl Med. 3, 103ra198 (2011). (PMID: 10.1126/scitranslmed.3002531)
Marx, C. et al. Eosinophil-platelet interactions promote atherosclerosis and stabilize thrombosis with eosinophil extracellular traps. Blood 134, 1859–1872 (2019). (PMID: 31481482690880610.1182/blood.2019000518)
Moosbauer, C. et al. Eosinophils are a major intravascular location for tissue factor storage and exposure. Blood 109, 995–1002 (2007). (PMID: 1700337910.1182/blood-2006-02-004945)
Uderhardt, S. et al. Enzymatic lipid oxidation by eosinophils propagates coagulation, hemostasis, and thrombotic disease. J. Exp. Med. 214, 2121–2138 (2017). (PMID: 28566277550242410.1084/jem.20161070)
Ames, P. R., Margaglione, M., Mackie, S. & Alves, J. D. Eosinophilia and thrombophilia in churg strauss syndrome: a clinical and pathogenetic overview. Clin. Appl. Thromb. Hemost. 16, 628–636 (2010). (PMID: 1983361810.1177/1076029609348647)
Cugno, M., Marzano, A. V., Lorini, M., Carbonelli, V. & Tedeschi, A. Enhanced tissue factor expression by blood eosinophils from patients with hypereosinophilia: a possible link with thrombosis. PLoS ONE 9, e111862 (2014). (PMID: 25375118422294410.1371/journal.pone.0111862)
Gao, S. J. et al. Hypereosinophilic syndrome presenting with multiple organ infiltration and deep venous thrombosis: a case report and literature review. Medicine 95, e4658 (2016). (PMID: 27583887500857110.1097/MD.0000000000004658)
Yousefi, S. et al. Catapult-like release of mitochondrial DNA by eosinophils contributes to antibacterial defense. Nat. Med. 14, 949–953 (2008). (PMID: 1869024410.1038/nm.1855)
Heit, J. A. et al. Predictors of recurrence after deep vein thrombosis and pulmonary embolism: a population-based cohort study. Arch. Intern. Med. 160, 761–768 (2000). (PMID: 1073727510.1001/archinte.160.6.761)
Prandoni, P. et al. The risk of recurrent venous thromboembolism after discontinuing anticoagulation in patients with acute proximal deep vein thrombosis or pulmonary embolism. A prospective cohort study in 1,626 patients. Haematologica 92, 199–205 (2007). (PMID: 1729656910.3324/haematol.10516)
Goldhaber, S. Z. & Bounameaux, H. Pulmonary embolism and deep vein thrombosis. Lancet 379, 1835–1846 (2012). (PMID: 2249482710.1016/S0140-6736(11)61904-1)
Nieto, J. A. et al. Fatal bleeding in patients receiving anticoagulant therapy for venous thromboembolism: findings from the RIETE registry. J. Thromb. Haemost. 8, 1216–1222 (2010). (PMID: 2034572710.1111/j.1538-7836.2010.03852.x)
Heit, J. A. Epidemiology of venous thromboembolism. Nat. Rev. Cardiol. 12, 464–474 (2015). (PMID: 26076949462429810.1038/nrcardio.2015.83)
Heit, J. A. et al. The epidemiology of venous thromboembolism in the community. Thromb. Haemost. 86, 452–463 (2001). (PMID: 1148703610.1055/s-0037-1616243)
Cohen, A. T. et al. Venous thromboembolism (VTE) in Europe. The number of VTE events and associated morbidity and mortality. Thromb. Haemost. 98, 756–764 (2007). (PMID: 1793879810.1160/TH07-03-0212)
Chiu, J. J. & Chien, S. Effects of disturbed flow on vascular endothelium: pathophysiological basis and clinical perspectives. Physiol. Rev. 91, 327–387 (2011). (PMID: 10.1152/physrev.00047.200921248169)
Mohan, S., Mohan, N., Valente, A. J. & Sprague, E. A. Regulation of low shear flow-induced HAEC VCAM-1 expression and monocyte adhesion. Am. J. Physiol. 276, C1100–C1107 (1999). (PMID: 1032995810.1152/ajpcell.1999.276.5.C1100)
Gupta, N. et al. Activation of NLRP3 inflammasome complex potentiates venous thrombosis in response to hypoxia. Proc. Natl Acad. Sci. USA 114, 4763–4768 (2017). (PMID: 28420787542282310.1073/pnas.1620458114)
Ponomaryov, T., Payne, H., Fabritz, L., Wagner, D. D. & Brill, A. Mast cells granular contents are crucial for deep vein thrombosis in mice. Circ. Res. 121, 941–950 (2017). (PMID: 28739590562308910.1161/CIRCRESAHA.117.311185)
Subramaniam, S. et al. Distinct contributions of complement factors to platelet activation and fibrin formation in venous thrombus development. Blood 129, 2291–2302 (2017). (PMID: 28223279539948510.1182/blood-2016-11-749879)
Yago, T., Liu, Z., Ahamed, J. & McEver, R. P. Cooperative PSGL-1 and CXCR2 signaling in neutrophils promotes deep vein thrombosis in mice. Blood 132, 1426–1437 (2018). (PMID: 30068506616176910.1182/blood-2018-05-850859)
Brill, A. et al. Neutrophil extracellular traps promote deep vein thrombosis in mice. J. Thromb. Haemost. 10, 136–144 (2012). (PMID: 22044575331965110.1111/j.1538-7836.2011.04544.x)
Venereau, E., Schiraldi, M., Uguccioni, M. & Bianchi, M. E. HMGB1 and leukocyte migration during trauma and sterile inflammation. Mol. Immunol. 55, 76–82 (2013). (PMID: 2320710110.1016/j.molimm.2012.10.037)
Magder, L. S. & Petri, M. Incidence of and risk factors for adverse cardiovascular events among patients with systemic lupus erythematosus. Am. J. Epidemiol. 176, 708–719 (2012). (PMID: 23024137357125010.1093/aje/kws130)
Leffler, J. et al. Neutrophil extracellular traps that are not degraded in systemic lupus erythematosus activate complement exacerbating the disease. J. Immunol. 188, 3522–3531 (2012). (PMID: 2234566610.4049/jimmunol.1102404)
Lood, C. et al. Increased C1q, C4 and C3 deposition on platelets in patients with systemic lupus erythematosus–a possible link to venous thrombosis? Lupus 21, 1423–1432 (2012). (PMID: 2287825610.1177/0961203312457210)
Espinosa, G. & Cervera, R. Antiphospholipid syndrome: frequency, main causes and risk factors of mortality. Nat. Rev. Rheumatol. 6, 296–300 (2010). (PMID: 2038656310.1038/nrrheum.2010.47)
Fischetti, F. et al. Thrombus formation induced by antibodies to β2-glycoprotein I is complement dependent and requires a priming factor. Blood 106, 2340–2346 (2005). (PMID: 1595628810.1182/blood-2005-03-1319)
Girardi, G. et al. Complement C5a receptors and neutrophils mediate fetal injury in the antiphospholipid syndrome. J. Clin. Invest. 112, 1644–1654 (2003). (PMID: 1466074128164310.1172/JCI200318817)
Girardi, G., Redecha, P. & Salmon, J. E. Heparin prevents antiphospholipid antibody-induced fetal loss by inhibiting complement activation. Nat. Med. 10, 1222–1226 (2004). (PMID: 1548985810.1038/nm1121)
Garcia-Romo, G. S. et al. Netting neutrophils are major inducers of type I IFN production in pediatric systemic lupus erythematosus. Sci. Transl Med. 3, 73ra20 (2011). (PMID: 21389264314383710.1126/scitranslmed.3001201)
Solomon, D. H. et al. Cardiovascular morbidity and mortality in women diagnosed with rheumatoid arthritis. Circulation 107, 1303–1307 (2003). (PMID: 1262895210.1161/01.CIR.0000054612.26458.B2)
Hannawi, S., Haluska, B., Marwick, T. H. & Thomas, R. Atherosclerotic disease is increased in recent-onset rheumatoid arthritis: a critical role for inflammation. Arthritis Res. Ther. 9, R116 (2007). (PMID: 17986352224623410.1186/ar2323)
Maradit-Kremers, H. et al. Increased unrecognized coronary heart disease and sudden deaths in rheumatoid arthritis: a population-based cohort study. Arthritis Rheum. 52, 402–411 (2005). (PMID: 1569301010.1002/art.20853)
Khandpur, R. et al. NETs are a source of citrullinated autoantigens and stimulate inflammatory responses in rheumatoid arthritis. Sci. Transl Med. 5, 178ra140 (2013). (PMID: 10.1126/scitranslmed.3005580)
Massberg, S. et al. A critical role of platelet adhesion in the initiation of atherosclerotic lesion formation. J. Exp. Med. 196, 887–896 (2002). (PMID: 12370251219402510.1084/jem.20012044)
Massberg, S. et al. Platelet adhesion via glycoprotein IIb integrin is critical for atheroprogression and focal cerebral ischemia: an in vivo study in mice lacking glycoprotein IIb. Circulation 112, 1180–1188 (2005). (PMID: 1610323510.1161/CIRCULATIONAHA.105.539221)
Gerdes, N. et al. Platelet CD40 exacerbates atherosclerosis by transcellular activation of endothelial cells and leukocytes. Arterioscler. Thromb. Vasc. Biol. 36, 482–490 (2016). (PMID: 2682195010.1161/ATVBAHA.115.307074)
Drechsler, M., Megens, R. T., van Zandvoort, M., Weber, C. & Soehnlein, O. Hyperlipidemia-triggered neutrophilia promotes early atherosclerosis. Circulation 122, 1837–1845 (2010). (PMID: 2095620710.1161/CIRCULATIONAHA.110.961714)
Koenen, R. R. et al. Disrupting functional interactions between platelet chemokines inhibits atherosclerosis in hyperlipidemic mice. Nat. Med. 15, 97–103 (2009). (PMID: 1912265710.1038/nm.1898)
Massberg, S. et al. Platelets secrete stromal cell-derived factor 1α and recruit bone marrow-derived progenitor cells to arterial thrombi in vivo. J. Exp. Med. 203, 1221–1233 (2006). (PMID: 16618794212120510.1084/jem.20051772)
Silvestre-Roig, C. et al. Externalized histone H4 orchestrates chronic inflammation by inducing lytic cell death. Nature 569, 236–240 (2019). (PMID: 31043745671652510.1038/s41586-019-1167-6)
Xia, G. L., Wang, Y. K. & Huang, Z. Q. The correlation of serum myeloid-related protein-8/14 and eosinophil cationic protein in patients with coronary artery disease. BioMed. Res. Int. 2016, 4980251 (2016). (PMID: 27022611478906110.1155/2016/4980251)
Niccoli, G. et al. Eosinophil cationic protein: a new biomarker of coronary atherosclerosis. Atherosclerosis 211, 606–611 (2010). (PMID: 2030788310.1016/j.atherosclerosis.2010.02.038)
Haley, K. J. et al. Overexpression of eotaxin and the CCR3 receptor in human atherosclerosis: using genomic technology to identify a potential novel pathway of vascular inflammation. Circulation 102, 2185–2189 (2000). (PMID: 1105609010.1161/01.CIR.102.18.2185)
Pertiwi, K. R. et al. Extracellular traps derived from macrophages, mast cells, eosinophils and neutrophils are generated in a time-dependent manner during atherothrombosis. J. Pathol. 247, 505–512 (2018). (PMID: 10.1002/path.5212)
van Dijk, R. A. et al. Systematic evaluation of the cellular innate immune response during the process of human atherosclerosis. J. Am. Heart Assoc. 5, e002860 (2016). (PMID: 27312803493725010.1161/JAHA.115.002860)
Novotny, J. et al. Thrombus NET content is associated with clinical outcome in stroke and myocardial infarction. Neurology 94, e2346–e2360 (2020). (PMID: 3243486510.1212/WNL.0000000000009532)
Gudbjartsson, D. F. et al. Sequence variants affecting eosinophil numbers associate with asthma and myocardial infarction. Nat. Genet. 41, 342–347 (2009). (PMID: 1919861010.1038/ng.323)
Pircher, J., Engelmann, B., Massberg, S. & Schulz, C. Platelet-neutrophil crosstalk in atherothrombosis. Thromb. Haemost. 119, 1274–1282 (2019). (PMID: 3125497510.1055/s-0039-1692983)
Tardif, J. C. et al. Effects of the P-selectin antagonist inclacumab on myocardial damage after percutaneous coronary intervention for non-ST-segment elevation myocardial infarction: results of the SELECT-ACS trial. J. Am. Coll. Cardiol. 61, 2048–2055 (2013). (PMID: 2350023010.1016/j.jacc.2013.03.003)
Dhanesha, N. et al. Targeting myeloid-cell specific integrin α9β1 inhibits arterial thrombosis in mice. Blood 135, 857–861 (2020). (PMID: 31951649706803310.1182/blood.2019002846)
Faraday, N. et al. Cathepsin G-dependent modulation of platelet thrombus formation in vivo by blood neutrophils. PLoS ONE 8, e71447 (2013). (PMID: 23940756373395810.1371/journal.pone.0071447)
Ortega-Gomez, A. et al. Cathepsin G controls arterial but not venular myeloid cell recruitment. Circulation 134, 1176–1188 (2016). (PMID: 27660294528800710.1161/CIRCULATIONAHA.116.024790)
Vogel, S. et al. Platelet-derived HMGB1 is a critical mediator of thrombosis. J. Clin. Invest. 125, 4638–4654 (2015). (PMID: 26551681466578510.1172/JCI81660)
Franck, G. et al. Roles of PAD4 and NETosis in experimental atherosclerosis and arterial injury: implications for superficial erosion. Circ. Res. 123, 33–42 (2018). (PMID: 29572206601487210.1161/CIRCRESAHA.117.312494)
Liu, Y. et al. Myeloid-specific deletion of peptidylarginine deiminase 4 mitigates atherosclerosis. Front. Immunol. 9, 1680 (2018). (PMID: 30140264609496610.3389/fimmu.2018.01680)
Novotny, J. et al. Histological comparison of arterial thrombi in mice and men and the influence of Cl-amidine on thrombus formation. PLoS ONE 13, e0190728 (2018). (PMID: 29293656574986210.1371/journal.pone.0190728)
Schreiber, A. et al. Necroptosis controls NET generation and mediates complement activation, endothelial damage, and autoimmune vasculitis. Proc. Natl Acad. Sci. USA 114, E9618–E9625 (2017). (PMID: 29078325569255410.1073/pnas.1708247114)
Wang, H., Wang, C., Zhao, M. H. & Chen, M. Neutrophil extracellular traps can activate alternative complement pathways. Clin. Exp. Immunol. 181, 518–527 (2015). (PMID: 25963026455738710.1111/cei.12654)
Gushiken, F. C., Han, H., Li, J., Rumbaut, R. E. & Afshar-Kharghan, V. Abnormal platelet function in C3-deficient mice. J. Thromb. Haemost. 7, 865–870 (2009). (PMID: 19291167286767310.1111/j.1538-7836.2009.03334.x)
Sauter, R. J. et al. Functional relevance of the anaphylatoxin receptor C3aR for platelet function and arterial thrombus formation marks an intersection point between innate immunity and thrombosis. Circulation 138, 1720–1735 (2018). (PMID: 29802205620224410.1161/CIRCULATIONAHA.118.034600)
Jaiswal, S. et al. Age-related clonal hematopoiesis associated with adverse outcomes. N. Engl. J. Med. 371, 2488–2498 (2014). (PMID: 25426837430666910.1056/NEJMoa1408617)
Jaiswal, S. et al. Clonal hematopoiesis and risk of atherosclerotic cardiovascular disease. N. Engl. J. Med. 377, 111–121 (2017). (PMID: 28636844671750910.1056/NEJMoa1701719)
Fuster, J. J. et al. Clonal hematopoiesis associated with TET2 deficiency accelerates atherosclerosis development in mice. Science 355, 842–847 (2017). (PMID: 28104796554205710.1126/science.aag1381)
James, C. et al. A unique clonal JAK2 mutation leading to constitutive signalling causes polycythaemia vera. Nature 434, 1144–1148 (2005). (PMID: 1579356110.1038/nature03546)
Wolach, O. et al. Increased neutrophil extracellular trap formation promotes thrombosis in myeloproliferative neoplasms. Sci. Transl Med. 10, eaan8292 (2018). (PMID: 29643232644246610.1126/scitranslmed.aan8292)
Wang, W. et al. Macrophage inflammation, erythrophagocytosis, and accelerated atherosclerosis in Jak2 (V617F) Mice. Circ. Res. 123, e35–e47 (2018). (PMID: 30571460630979610.1161/CIRCRESAHA.118.313283)
Cull, A. H., Snetsinger, B., Buckstein, R., Wells, R. A. & Rauh, M. J. Tet2 restrains inflammatory gene expression in macrophages. Exp. Hematol. 55, 56–70 (2017). (PMID: 2882685910.1016/j.exphem.2017.08.001)
Zhang, Q. et al. Tet2 is required to resolve inflammation by recruiting Hdac2 to specifically repress IL-6. Nature 525, 389–393 (2015). (PMID: 26287468469774710.1038/nature15252)
Veninga, A., De Simone, I., Heemskerk, J. W. M., Cate, H. T. & van der Meijden, P. E. J. Clonal hematopoietic mutations linked to platelet traits and the risk of thrombosis or bleeding. Haematologica 105, 2020–2031 (2020). (PMID: 32554558739529010.3324/haematol.2019.235994)
Bonaca, M. P. et al. Rivaroxaban in peripheral artery disease after revascularization. N. Engl. J. Med. 382, 1994–2004 (2020). (PMID: 3222213510.1056/NEJMoa2000052)
Borissoff, J. I., Spronk, H. M. & ten Cate, H. The hemostatic system as a modulator of atherosclerosis. N. Engl. J. Med. 364, 1746–1760 (2011). (PMID: 2154274510.1056/NEJMra1011670)
Eikelboom, J. W. et al. Rivaroxaban with or without aspirin in stable cardiovascular disease. N. Engl. J. Med. 377, 1319–1330 (2017). (PMID: 2884419210.1056/NEJMoa1709118)
Gadi, I. et al. Different DOACs control inflammation in cardiac ischemia-reperfusion differently. Circ. Res. 128, 513–529 (2020). (PMID: 3335337310.1161/CIRCRESAHA.120.3172198293866)
Hara, T. et al. Rivaroxaban, a novel oral anticoagulant, attenuates atherosclerotic plaque progression and destabilization in ApoE-deficient mice. Atherosclerosis 242, 639–646 (2015). (PMID: 2581732910.1016/j.atherosclerosis.2015.03.023)
Vu, T. K., Hung, D. T., Wheaton, V. I. & Coughlin, S. R. Molecular cloning of a functional thrombin receptor reveals a novel proteolytic mechanism of receptor activation. Cell 64, 1057–1068 (1991). (PMID: 167226510.1016/0092-8674(91)90261-V)
Nidorf, S. M. et al. Colchicine in patients with chronic coronary disease. N. Engl. J. Med. 383, 1838–1847 (2020). (PMID: 3286538010.1056/NEJMoa2021372)
Ridker, P. M. et al. Antiinflammatory therapy with canakinumab for atherosclerotic disease. N. Engl. J. Med. 377, 1119–1131 (2017). (PMID: 2884575110.1056/NEJMoa1707914)
Tardif, J. C. et al. Efficacy and safety of low-dose colchicine after myocardial infarction. N. Engl. J. Med. 381, 2497–2505 (2019). (PMID: 3173314010.1056/NEJMoa1912388)
Kirchhof, P. et al. Effects of rivaroxaban on biomarkers of coagulation and inflammation: a post hoc analysis of the X-VeRT TRIAL. TH Open 4, e20–e32 (2020). (PMID: 31984306697817710.1055/s-0040-1701206)
Busch, G. et al. Coagulation factor Xa stimulates interleukin-8 release in endothelial cells and mononuclear leukocytes: implications in acute myocardial infarction. Arterioscler. Thromb. Vasc. Biol. 25, 461–466 (2005). (PMID: 1555069610.1161/01.ATV.0000151279.35780.2d)
Daubie, V. et al. Factor Xa and thrombin evoke additive calcium and proinflammatory responses in endothelial cells subjected to coagulation. Biochim. Biophys. Acta 1763, 860–869 (2006). (PMID: 1676546610.1016/j.bbamcr.2006.04.010)
Senden, N. H. et al. Factor Xa induces cytokine production and expression of adhesion molecules by human umbilical vein endothelial cells. J. Immunol. 161, 4318–4324 (1998). (PMID: 978020810.4049/jimmunol.161.8.4318)
Ichikawa, H. et al. Rivaroxaban, a direct factor Xa inhibitor, ameliorates hypertensive renal damage through inhibition of the inflammatory response mediated by protease-activated receptor pathway. J. Am. Heart Assoc. 8, e012195 (2019). (PMID: 30957622650718710.1161/JAHA.119.012195)
Wildhagen, K. C. et al. Nonanticoagulant heparin prevents histone-mediated cytotoxicity in vitro and improves survival in sepsis. Blood 123, 1098–1101 (2014). (PMID: 2426423110.1182/blood-2013-07-514984)
Mansour, A., Bachelot-Loza, C., Nesseler, N., Gaussem, P. & Gouin-Thibault, I. P2Y12 inhibition beyond thrombosis: effects on inflammation. Int. J. Mol. Sci. 21, 1391 (2020). (PMID: 707304010.3390/ijms21041391)
Mackman, N., Bergmeier, W., Stouffer, G. A. & Weitz, J. I. Therapeutic strategies for thrombosis: new targets and approaches. Nat. Rev. Drug Discov. 19, 333–352 (2020). (PMID: 3213267810.1038/s41573-020-0061-0)
Jeong, H. S. et al. Comparison of ticagrelor versus prasugrel for inflammation, vascular function, and circulating endothelial progenitor cells in diabetic patients with non-ST-segment elevation acute coronary syndrome requiring coronary stenting: a prospective, randomized, crossover trial. JACC Cardiovasc. Interv. 10, 1646–1658 (2017). (PMID: 2883847510.1016/j.jcin.2017.05.064)
Morris, T. et al. Effects of low-dose aspirin on acute inflammatory responses in humans. J. Immunol. 183, 2089–2096 (2009). (PMID: 1959700210.4049/jimmunol.0900477)
Paul-Clark, M. J., Van Cao, T., Moradi-Bidhendi, N., Cooper, D. & Gilroy, D. W. 15-epi-lipoxin A4-mediated induction of nitric oxide explains how aspirin inhibits acute inflammation. J. Exp. Med. 200, 69–78 (2004). (PMID: 15238606221331110.1084/jem.20040566)
Dutta, P. et al. Myocardial infarction accelerates atherosclerosis. Nature 487, 325–329 (2012). (PMID: 22763456340132610.1038/nature11260)
Sager, H. B. et al. Targeting interleukin-1β reduces leukocyte production after acute myocardial infarction. Circulation 132, 1880–1890 (2015). (PMID: 26358260465179510.1161/CIRCULATIONAHA.115.016160)
Gomez, D. et al. Interleukin-1β has atheroprotective effects in advanced atherosclerotic lesions of mice. Nat. Med. 24, 1418–1429 (2018). (PMID: 30038218613082210.1038/s41591-018-0124-5)
Alexander, M. R. et al. Genetic inactivation of IL-1 signaling enhances atherosclerotic plaque instability and reduces outward vessel remodeling in advanced atherosclerosis in mice. J. Clin. Invest. 122, 70–79 (2012). (PMID: 2220168110.1172/JCI43713)
Ridker, P. M. et al. Low-dose methotrexate for the prevention of atherosclerotic events. N. Engl. J. Med. 380, 752–762 (2019). (PMID: 3041561010.1056/NEJMoa1809798)
Munoz, L. E. et al. Neutrophil extracellular traps initiate gallstone formation. Immunity 51, 443–450 (2019). (PMID: 3142287010.1016/j.immuni.2019.07.002)
Martinon, F., Petrilli, V., Mayor, A., Tardivel, A. & Tschopp, J. Gout-associated uric acid crystals activate the NALP3 inflammasome. Nature 440, 237–241 (2006). (PMID: 1640788910.1038/nature04516)
Opstal, T. S. J. et al. Colchicine attenuates inflammation beyond the inflammasome in chronic coronary artery disease: a LoDoCo2 proteomic substudy. Circulation 142, 1996–1998 (2020). (PMID: 3286499810.1161/CIRCULATIONAHA.120.050560)
Castro, M. et al. Reslizumab for inadequately controlled asthma with elevated blood eosinophil counts: results from two multicentre, parallel, double-blind, randomised, placebo-controlled, phase 3 trials. Lancet Respir. Med. 3, 355–366 (2015). (PMID: 2573699010.1016/S2213-2600(15)00042-9)
FitzGerald, J. M. et al. Benralizumab, an anti-interleukin-5 receptor α monoclonal antibody, as add-on treatment for patients with severe, uncontrolled, eosinophilic asthma (CALIMA): a randomised, double-blind, placebo-controlled phase 3 trial. Lancet 388, 2128–2141 (2016). (PMID: 2760940610.1016/S0140-6736(16)31322-8)
Ortega, H. G. et al. Mepolizumab treatment in patients with severe eosinophilic asthma. N. Engl. J. Med. 371, 1198–1207 (2014). (PMID: 2519905910.1056/NEJMoa1403290)
Mastellos, D. C., Ricklin, D. & Lambris, J. D. Clinical promise of next-generation complement therapeutics. Nat. Rev. Drug Discov. 18, 707–729 (2019). (PMID: 31324874734085310.1038/s41573-019-0031-6)
Liverani, E., Rico, M. C., Tsygankov, A. Y., Kilpatrick, L. E. & Kunapuli, S. P. P2Y12 receptor modulates sepsis-induced inflammation. Arterioscler. Thromb. Vasc. Biol. 36, 961–971 (2016). (PMID: 27055904485011310.1161/ATVBAHA.116.307401)
Sexton, T. R. et al. Ticagrelor reduces thromboinflammatory markers in patients with pneumonia. JACC Basic Transl. Sci. 3, 435–449 (2018). (PMID: 30175268611570310.1016/j.jacbts.2018.05.005)
Hillmen, P. et al. Effect of the complement inhibitor eculizumab on thromboembolism in patients with paroxysmal nocturnal hemoglobinuria. Blood 110, 4123–4128 (2007). (PMID: 1770289710.1182/blood-2007-06-095646)
Dong, Y. et al. TLR4 regulates ROS and autophagy to control neutrophil extracellular traps formation against Streptococcus pneumoniae in acute otitis media. Pediatr. Res. https://doi.org/10.1038/s41390-020-0964-9 (2020). (PMID: 10.1038/s41390-020-0964-9327267997855434)
Guglietta, S. et al. Coagulation induced by C3aR-dependent NETosis drives protumorigenic neutrophils during small intestinal tumorigenesis. Nat. Commun. 7, 11037 (2016). (PMID: 26996437480216910.1038/ncomms11037)
Metzler, K. D., Goosmann, C., Lubojemska, A., Zychlinsky, A. & Papayannopoulos, V. A myeloperoxidase-containing complex regulates neutrophil elastase release and actin dynamics during NETosis. Cell Rep. 8, 883–896 (2014). (PMID: 25066128447168010.1016/j.celrep.2014.06.044)
Papayannopoulos, V., Metzler, K. D., Hakkim, A. & Zychlinsky, A. Neutrophil elastase and myeloperoxidase regulate the formation of neutrophil extracellular traps. J. Cell Biol. 191, 677–691 (2010). (PMID: 20974816300330910.1083/jcb.201006052)
Vu, T. T. et al. Histidine-rich glycoprotein binds DNA and RNA and attenuates their capacity to activate the intrinsic coagulation pathway. Thromb. Haemost. 115, 89–98 (2016). (PMID: 2635485710.1160/TH15-04-0336)
Fu, H. et al. Flow-induced elongation of von willebrand factor precedes tension-dependent activation. Nat. Commun. 8, 324 (2017). (PMID: 28831047556734310.1038/s41467-017-00230-2)
Jiang, Y., Fu, H., Springer, T. A. & Wong, W. P. Electrostatic steering enables flow-activated von willebrand factor to bind platelet glycoprotein, revealed by single-molecule stretching and imaging. J. Mol. Biol. 431, 1380–1396 (2019). (PMID: 30797858693611010.1016/j.jmb.2019.02.014)
Chonn, A., Cullis, P. R. & Devine, D. V. The role of surface charge in the activation of the classical and alternative pathways of complement by liposomes. J. Immunol. 146, 4234–4241 (1991). (PMID: 204079810.4049/jimmunol.146.12.4234)
Substance Nomenclature:
0 (Anti-Inflammatory Agents)
0 (Fibrinolytic Agents)
0 (Inflammation Mediators)
Entry Date(s):
Date Created: 20210507 Date Completed: 20210825 Latest Revision: 20230201
Update Code:
20240104
PubMed Central ID:
PMC8100938
DOI:
10.1038/s41569-021-00552-1
PMID:
33958774
Czasopismo naukowe
Thrombosis is the most feared complication of cardiovascular diseases and a main cause of death worldwide, making it a major health-care challenge. Platelets and the coagulation cascade are effectively targeted by antithrombotic approaches, which carry an inherent risk of bleeding. Moreover, antithrombotics cannot completely prevent thrombotic events, implicating a therapeutic gap due to a third, not yet adequately addressed mechanism, namely inflammation. In this Review, we discuss how the synergy between inflammation and thrombosis drives thrombotic diseases. We focus on the huge potential of anti-inflammatory strategies to target cardiovascular pathologies. Findings in the past decade have uncovered a sophisticated connection between innate immunity, platelet activation and coagulation, termed immunothrombosis. Immunothrombosis is an important host defence mechanism to limit systemic spreading of pathogens through the bloodstream. However, the aberrant activation of immunothrombosis in cardiovascular diseases causes myocardial infarction, stroke and venous thromboembolism. The clinical relevance of aberrant immunothrombosis, referred to as thromboinflammation, is supported by the increased risk of cardiovascular events in patients with inflammatory diseases but also during infections, including in COVID-19. Clinical trials in the past 4 years have confirmed the anti-ischaemic effects of anti-inflammatory strategies, backing the concept of a prothrombotic function of inflammation. Targeting inflammation to prevent thrombosis leaves haemostasis mainly unaffected, circumventing the risk of bleeding associated with current approaches. Considering the growing number of anti-inflammatory therapies, it is crucial to appreciate their potential in covering therapeutic gaps in cardiovascular diseases.
(© 2021. Springer Nature Limited.)

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