Coronavirus (Covid-19) sepsis: revisiting mitochondrial dysfunction in pathogenesis, aging, inflammation, and mortality.

Szczegóły
Abstrakt

Tytuł:: Coronavirus (Covid-19) sepsis: revisiting mitochondrial dysfunction in pathogenesis, aging, inflammation, and mortality.
Autorzy:: Shenoy S; Department of Surgery, Kansas City VA Medical Center, University of Missouri Kansas City, 4801 E Linwood Blvd, Kansas City, MO, 64128, USA. .
Źródło:: Inflammation research : official journal of the European Histamine Research Society ... [et al.] [Inflamm Res] 2020 Nov; Vol. 69 (11), pp. 1077-1085. Date of Electronic Publication: 2020 Aug 07.
Typ publikacji:: Journal Article; Review
Język:: English
Imprint Name(s):: Original Publication: Basel, Switzerland : Birkhäuser, c1995-
MeSH Terms:: Coronavirus Infections/*complications
Coronavirus Infections/*pathology
Inflammation/*etiology
Inflammation/*pathology
Mitochondria/*metabolism
Mitochondria/*pathology
Mitochondrial Diseases/*etiology
Mitochondrial Diseases/*pathology
Pneumonia, Viral/*complications
Pneumonia, Viral/*pathology
Sepsis/*etiology
Sepsis/*pathology
Aging ; COVID-19 ; Coronavirus Infections/mortality ; Humans ; Inflammation/mortality ; Mitochondrial Diseases/mortality ; Pandemics ; Pneumonia, Viral/mortality ; Sepsis/mortality
References:: Lancet. 2002 Jul 20;360(9328):219-23. (PMID: 12133657)
Lancet Infect Dis. 2020 Jun;20(6):656-657. (PMID: 32199493)
Immunity. 2020 Jun 16;52(6):910-941. (PMID: 32505227)
CMAJ. 2004 Nov 23;171(11):1349-52. (PMID: 15557587)
Signal Transduct Target Ther. 2020 Mar 27;5(1):33. (PMID: 32296069)
N Engl J Med. 2020 Mar 19;382(12):1177-1179. (PMID: 32074444)
Crit Care Res Pract. 2018 Nov 8;2018:5489571. (PMID: 30533222)
Ageing Res Rev. 2015 Nov;24(Pt A):83-97. (PMID: 26200296)
Crit Care. 2012;16(4):R120. (PMID: 22781303)
EBioMedicine. 2020 May;55:102763. (PMID: 32361250)
Shock. 2013 Jan;39(1):113-4. (PMID: 23247128)
Nature. 2010 Mar 4;464(7285):104-7. (PMID: 20203610)
Front Immunol. 2018 May 08;9:891. (PMID: 29867926)
PLoS Med. 2013 Dec;10(12):e1001577; discussion e1001577. (PMID: 24391478)
Genetics. 2017 Nov;207(3):843-871. (PMID: 29097398)
Nature. 2015 Apr 23;520(7548):553-7. (PMID: 25642965)
J Cell Biol. 2011 May 30;193(5):809-18. (PMID: 21606204)
Cell Syst. 2020 Jul 22;11(1):102-108.e3. (PMID: 32673562)
Obesity (Silver Spring). 2015 Jun;23(6):1209-17. (PMID: 25959124)
JAMA. 2016 Feb 23;315(8):801-10. (PMID: 26903338)
Nat Rev Mol Cell Biol. 2016 Nov;17(11):679-690. (PMID: 27552971)
Cell Discov. 2020 Feb 24;6:11. (PMID: 32133153)
JAMA. 2020 Mar 17;323(11):1061-1069. (PMID: 32031570)
Aging (Albany NY). 2020 May 29;12(10):9959-9981. (PMID: 32470948)
Virulence. 2014 Jan 1;5(1):66-72. (PMID: 24185508)
PLoS One. 2015 Oct 08;10(10):e0139416. (PMID: 26448624)
Front Mol Biosci. 2019 Sep 06;6:85. (PMID: 31555665)
PLoS Biol. 2008 Sep 16;6(9):e226. (PMID: 18798692)
J Virol. 2012 May;86(10):5808-16. (PMID: 22438542)
J Clin Virol. 2017 Jan;86:14-19. (PMID: 27893998)
J Immunol. 2014 Sep 15;193(6):3080-9. (PMID: 25135833)
J Leukoc Biol. 2014 Nov;96(5):785-96. (PMID: 25001863)
Int J Mol Sci. 2018 Sep 13;19(9):. (PMID: 30216989)
Mol Cell. 2016 Mar 3;61(5):654-666. (PMID: 26942670)
Nucleic Acids Res. 2009 May;37(8):2539-48. (PMID: 19264794)
N Engl J Med. 2020 Mar 26;382(13):1268-1269. (PMID: 32109011)
J Biol Chem. 2020 Dec 25;295(52):17986-17996. (PMID: 33051211)
J Virol. 2007 Jan;81(2):548-57. (PMID: 17108024)
Cell Death Differ. 2016 Mar;23(3):369-79. (PMID: 26794443)
FEBS J. 2020 Apr;287(8):1478-1495. (PMID: 31970890)
Front Genet. 2021 Mar 16;12:599261. (PMID: 33796130)
Proc Natl Acad Sci U S A. 2020 Apr 28;117(17):9490-9496. (PMID: 32253318)
Curr Opin Crit Care. 2017 Aug;23(4):284-290. (PMID: 28562385)
Cell. 2020 Apr 16;181(2):271-280.e8. (PMID: 32142651)
J Infect. 2016 Dec;73(6):598-606. (PMID: 27615557)
Rev Med Virol. 2020 May;30(3):e2109. (PMID: 32314850)
Am J Physiol Cell Physiol. 2020 Aug 1;319(2):C258-C267. (PMID: 32510973)
J Cell Biol. 1994 Sep;126(6):1353-60. (PMID: 8089170)
Nature. 2020 Jul;583(7816):459-468. (PMID: 32353859)
Expert Opin Ther Targets. 2020 May;24(5):489-497. (PMID: 32174215)
Contributed Indexing:: Keywords: Covid-19; DAMP; HIF-α; Mitochondrial dysfunction; Sirtuins; Viral replication
Entry Date(s):: Date Created: 20200809 Date Completed: 20201001 Latest Revision: 20220218
Update Code:: 20240105
PubMed Central ID:: PMC7410962
DOI:: 10.1007/s00011-020-01389-z
PMID:: 32767095
: Czasopismo naukowe

Full Text Finder

Background: Decline in mitochondrial function occurs with aging and may increase mortality. We discuss mitochondrial contribution to Covid-19 sepsis, specifically the complex interaction of innate immune function, viral replication, hyper-inflammatory state, and HIF-α/Sirtuin pathways.
Methods: Articles from PubMed/Medline searches were reviewed using the combination of terms "SARS-CoV-2, Covid-19, sepsis, mitochondria, aging, and immunometabolism".
Results: Evidence indicates that mitochondria in senescent cells may be dysfunctional and unable to keep up with hypermetabolic demands associated with Covid-19 sepsis. Mitochondrial proteins may serve as damage-associated molecular pattern (DAMP) activating innate immunity. Disruption in normal oxidative phosphorylation pathways contributes to elevated ROS which activates sepsis cascade through HIF-α/Sirtuin pathway. Viral-mitochondrial interaction may be necessary for replication and increased viral load. Hypoxia and hyper-inflammatory state contribute to increased mortality associated with Covid-19 sepsis.
Conclusions: Aging is associated with worse outcomes in sepsis. Modulating Sirtuin activity is emerging as therapeutic agent in sepsis. HIF-α, levels of mitochondrial DNA, and other mitochondrial DAMP molecules may also serve as useful biomarker and need to be investigated. These mechanisms should be explored specifically for Covid-19-related sepsis. Understanding newly discovered regulatory mechanisms may lead to the development of novel diagnostic and therapeutic targets.

Informacja