Growth differentiation factor 11 induces skeletal muscle atrophy via a STAT3-dependent mechanism in pulmonary arterial hypertension.

Tytuł:: Growth differentiation factor 11 induces skeletal muscle atrophy via a STAT3-dependent mechanism in pulmonary arterial hypertension.
Autorzy:: Xiang G; Department of Pulmonary and Critical Care Medicine, Zhongshan Hospital, Fudan University, 180 Fenglin Road, Shanghai, 200032, China.
Ying K; Department of Pulmonary and Critical Care Medicine, Zhongshan Hospital, Fudan University, 180 Fenglin Road, Shanghai, 200032, China.
Jiang P; Department of Pulmonary and Critical Care Medicine, Zhongshan Hospital, Fudan University, 180 Fenglin Road, Shanghai, 200032, China.
Jia M; Department of Pulmonary and Critical Care Medicine, Zhongshan Hospital, Fudan University, 180 Fenglin Road, Shanghai, 200032, China.
Sun Y; Department of Pulmonary and Critical Care Medicine, Zhongshan Hospital, Fudan University, 180 Fenglin Road, Shanghai, 200032, China.
Li S; Department of Pulmonary and Critical Care Medicine, Zhongshan Hospital, Fudan University, 180 Fenglin Road, Shanghai, 200032, China. .
Wu X; Department of Pulmonary and Critical Care Medicine, Zhongshan Hospital, Fudan University, 180 Fenglin Road, Shanghai, 200032, China. follow_the_.
Hao S; Department of Pulmonary and Critical Care Medicine, Zhongshan Hospital, Fudan University, 180 Fenglin Road, Shanghai, 200032, China. .
Źródło:: Skeletal muscle [Skelet Muscle] 2022 May 06; Vol. 12 (1), pp. 10. Date of Electronic Publication: 2022 May 06.
Typ publikacji:: Journal Article; Research Support, Non-U.S. Gov't
Język:: English
Imprint Name(s):: Original Publication: [London] : BioMed Central Ltd., 2011-
MeSH Terms:: Growth Differentiation Factors*/genetics
Growth Differentiation Factors*/metabolism
Muscular Atrophy*/metabolism
Pulmonary Arterial Hypertension*
STAT3 Transcription Factor*/metabolism
Bone Morphogenetic Proteins/metabolism ; Humans ; Muscle, Skeletal/metabolism ; Muscle, Skeletal/pathology
References:: Am J Respir Cell Mol Biol. 2014 Jan;50(1):74-86. (PMID: 23972212)
JCI Insight. 2020 Mar 26;5(6):. (PMID: 32078585)
Cell Metab. 2016 Jun 14;23(6):1207-1215. (PMID: 27304512)
Circ Res. 2015 Jan 2;116(1):56-69. (PMID: 25287062)
EMBO Mol Med. 2017 Apr;9(4):531-544. (PMID: 28270449)
Mol Ther. 2016 Nov;24(11):1926-1938. (PMID: 27502608)
Exp Mol Med. 2018 Apr 27;50(4):1-11. (PMID: 29700287)
J Am Soc Nephrol. 2009 Mar;20(3):604-12. (PMID: 19158350)
Cell. 2004 Apr 30;117(3):399-412. (PMID: 15109499)
Int J Chron Obstruct Pulmon Dis. 2012;7:523-35. (PMID: 22973093)
Semin Cell Dev Biol. 2016 Jun;54:28-41. (PMID: 26860754)
Qual Life Res. 2006 Feb;15(1):103-15. (PMID: 16411035)
Cell Metab. 2013 Sep 3;18(3):368-79. (PMID: 24011072)
Nat Med. 2014 Nov;20(11):1289-300. (PMID: 25344740)
J Mol Cell Cardiol. 1998 Nov;30(11):2449-59. (PMID: 9925379)
Mol Cell Biol. 2005 Aug;25(15):6533-45. (PMID: 16024790)
Eur Respir J. 2005 Jan;25(1):125-30. (PMID: 15640333)
Immunol Endocr Metab Agents Med Chem. 2010;10:183-194. (PMID: 21423813)
Cell. 2016 Mar 10;164(6):1248-1256. (PMID: 26967290)
Hypertension. 2018 Apr;71(4):729-741. (PMID: 29463625)
Ann Rheum Dis. 2016 Apr;76(4):748-755. (PMID: 27789465)
BMC Biol. 2017 Mar 3;15(1):19. (PMID: 28257634)
Nat Cell Biol. 2003 Feb;5(2):87-90. (PMID: 12563267)
J Cardiopulm Rehabil Prev. 2013 Sep-Oct;33(5):263-73. (PMID: 23962982)
Crit Rev Biochem Mol Biol. 2014 Jan-Feb;49(1):59-68. (PMID: 24237131)
Diabetes. 2013 Feb;62(2):457-65. (PMID: 23043161)
Oncogene. 2017 May 25;36(21):3059-3066. (PMID: 27893707)
EMBO Mol Med. 2017 May;9(5):622-637. (PMID: 28264935)
J Biol Chem. 2015 Apr 24;290(17):11177-87. (PMID: 25787076)
Ann Neurol. 2008 May;63(5):561-71. (PMID: 18335515)
Aging Clin Exp Res. 2010 Feb;22(1):24-30. (PMID: 19920407)
Respir Med. 2007 Nov;101(11):2366-9. (PMID: 17689235)
Int J Mol Sci. 2021 May 07;22(9):. (PMID: 34067108)
Thorax. 2019 Feb;74(2):164-176. (PMID: 30554141)
Exp Physiol. 2013 Aug;98(8):1262-6. (PMID: 23645549)
Nat Med. 2013 Jan;19(1):74-82. (PMID: 23263626)
Basic Res Cardiol. 2019 Mar 21;114(3):20. (PMID: 30900023)
Cancer Res. 2016 Jun 1;76(11):3397-410. (PMID: 27197172)
J Mol Histol. 2010 Feb;41(1):81-7. (PMID: 20349269)
Cancers (Basel). 2019 Nov 25;11(12):. (PMID: 31769424)
Cell Rep. 2018 Feb 6;22(6):1522-1530. (PMID: 29425507)
Sci Transl Med. 2020 May 13;12(543):. (PMID: 32404506)
Biochim Biophys Acta. 2015 Dec;1852(12):2722-31. (PMID: 26456917)
Contributed Indexing:: Keywords: GDF11; Pulmonary arterial hypertension; STAT3; Skeletal muscle atrophy
Substance Nomenclature:: 0 (Bone Morphogenetic Proteins)
0 (GDF11 protein, human)
0 (Growth Differentiation Factors)
0 (STAT3 Transcription Factor)
0 (STAT3 protein, human)
Entry Date(s):: Date Created: 20220507 Date Completed: 20220510 Latest Revision: 20220716
Update Code:: 20240105
PubMed Central ID:: PMC9074369
DOI:: 10.1186/s13395-022-00292-x
PMID:: 35524286
: Czasopismo naukowe

Pełny tekst

Skeletal muscle wasting is a clinically remarkable phenotypic feature of pulmonary arterial hypertension (PAH) that increases the risk of mortality. Growth differentiation factor 11 (GDF11), centrally involved in PAH pathogenesis, has an inhibitory effect on skeletal muscle growth in other conditions. However, whether GDF11 is involved in the pathogenesis of skeletal muscle wasting in PAH remains unknown. We showed that serum GDF11 levels in patients were increased following PAH. Skeletal muscle wasting in the MCT-treated PAH model is accompanied by an increase in circulating GDF11 levels and local catabolic markers (Fbx32, Trim63, Foxo1, and protease activity). In vitro GDF11 activated phosphorylation of STAT3. Antagonizing STAT3, with Stattic, in vitro and in vivo, could partially reverse proteolytic pathways including STAT3/socs3 and iNOS/NO in GDF11-meditated muscle wasting. Our findings demonstrate that GDF11 contributes to muscle wasting and the inhibition of its downstream molecule STAT3 shows promise as a therapeutic intervention by which muscle atrophy may be directly prevented in PAH.
(© 2022. The Author(s).)

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