Deficiency of myostatin protects skeletal muscle cells from ischemia reperfusion injury

Abstract Ischemia reperfusion (IR) injury plays a pivotal role in many diseases and leads to collateral damage during surgical interventions. While most studies focus on alleviating its severity in the context of brain, liver, kidney, and cardiac tissue, research as regards to skeletal muscle has no...

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Autores principales:	Christoph Wallner, Marius Drysch, Mustafa Becerikli, Sonja Verena Schmidt, Stephan Hahn, Johannes Maximilian Wagner, Felix Reinkemeier, Mehran Dadras, Alexander Sogorski, Maxi von Glinski, Marcus Lehnhardt, Björn Behr
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2021
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/12c03f6a0e564802b15ce6b2140494d4
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spelling	oai:doaj.org-article:12c03f6a0e564802b15ce6b2140494d42021-12-02T17:23:26ZDeficiency of myostatin protects skeletal muscle cells from ischemia reperfusion injury10.1038/s41598-021-92159-22045-2322https://doaj.org/article/12c03f6a0e564802b15ce6b2140494d42021-06-01T00:00:00Zhttps://doi.org/10.1038/s41598-021-92159-2https://doaj.org/toc/2045-2322Abstract Ischemia reperfusion (IR) injury plays a pivotal role in many diseases and leads to collateral damage during surgical interventions. While most studies focus on alleviating its severity in the context of brain, liver, kidney, and cardiac tissue, research as regards to skeletal muscle has not been conducted to the same extent. In the past, myostatin (MSTN), primarily known for supressing muscle growth, has been implicated in inflammatory circuits, and research provided promising results for cardiac IR injury mitigation by inhibiting MSTN cell surface receptor ACVR2B. This generated the question if interrupting MSTN signaling could temper IR injury in skeletal muscle. Examining human specimens from free myocutaneous flap transfer demonstrated increased MSTN signaling and tissue damage in terms of apoptotic activity, cell death, tissue edema, and lipid peroxidation. In subsequent in vivo Mstn Ln/Ln IR injury models, we identified potential mechanisms linking MSTN deficiency to protective effects, among others, inhibition of p38 MAPK signaling and SERCA2a modulation. Furthermore, transcriptional profiling revealed a putative involvement of NK cells. Collectively, this work establishes a protective role of MSTN deficiency in skeletal muscle IR injury.Christoph WallnerMarius DryschMustafa BecerikliSonja Verena SchmidtStephan HahnJohannes Maximilian WagnerFelix ReinkemeierMehran DadrasAlexander SogorskiMaxi von GlinskiMarcus LehnhardtBjörn BehrNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 11, Iss 1, Pp 1-12 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Christoph Wallner Marius Drysch Mustafa Becerikli Sonja Verena Schmidt Stephan Hahn Johannes Maximilian Wagner Felix Reinkemeier Mehran Dadras Alexander Sogorski Maxi von Glinski Marcus Lehnhardt Björn Behr Deficiency of myostatin protects skeletal muscle cells from ischemia reperfusion injury
description	Abstract Ischemia reperfusion (IR) injury plays a pivotal role in many diseases and leads to collateral damage during surgical interventions. While most studies focus on alleviating its severity in the context of brain, liver, kidney, and cardiac tissue, research as regards to skeletal muscle has not been conducted to the same extent. In the past, myostatin (MSTN), primarily known for supressing muscle growth, has been implicated in inflammatory circuits, and research provided promising results for cardiac IR injury mitigation by inhibiting MSTN cell surface receptor ACVR2B. This generated the question if interrupting MSTN signaling could temper IR injury in skeletal muscle. Examining human specimens from free myocutaneous flap transfer demonstrated increased MSTN signaling and tissue damage in terms of apoptotic activity, cell death, tissue edema, and lipid peroxidation. In subsequent in vivo Mstn Ln/Ln IR injury models, we identified potential mechanisms linking MSTN deficiency to protective effects, among others, inhibition of p38 MAPK signaling and SERCA2a modulation. Furthermore, transcriptional profiling revealed a putative involvement of NK cells. Collectively, this work establishes a protective role of MSTN deficiency in skeletal muscle IR injury.
format	article
author	Christoph Wallner Marius Drysch Mustafa Becerikli Sonja Verena Schmidt Stephan Hahn Johannes Maximilian Wagner Felix Reinkemeier Mehran Dadras Alexander Sogorski Maxi von Glinski Marcus Lehnhardt Björn Behr
author_facet	Christoph Wallner Marius Drysch Mustafa Becerikli Sonja Verena Schmidt Stephan Hahn Johannes Maximilian Wagner Felix Reinkemeier Mehran Dadras Alexander Sogorski Maxi von Glinski Marcus Lehnhardt Björn Behr
author_sort	Christoph Wallner
title	Deficiency of myostatin protects skeletal muscle cells from ischemia reperfusion injury
title_short	Deficiency of myostatin protects skeletal muscle cells from ischemia reperfusion injury
title_full	Deficiency of myostatin protects skeletal muscle cells from ischemia reperfusion injury
title_fullStr	Deficiency of myostatin protects skeletal muscle cells from ischemia reperfusion injury
title_full_unstemmed	Deficiency of myostatin protects skeletal muscle cells from ischemia reperfusion injury
title_sort	deficiency of myostatin protects skeletal muscle cells from ischemia reperfusion injury
publisher	Nature Portfolio
publishDate	2021
url	https://doaj.org/article/12c03f6a0e564802b15ce6b2140494d4
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Deficiency of myostatin protects skeletal muscle cells from ischemia reperfusion injury

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