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Medientyp:
E-Artikel
Titel:
Deficiency of myostatin protects skeletal muscle cells from ischemia reperfusion injury
Beteiligte:
Wallner, Christoph;
Drysch, Marius;
Becerikli, Mustafa;
Schmidt, Sonja Verena;
Hahn, Stephan;
Wagner, Johannes Maximilian;
Reinkemeier, Felix;
Dadras, Mehran;
Sogorski, Alexander;
von Glinski, Maxi;
Lehnhardt, Marcus;
Behr, Björn
Erschienen:
Springer Science and Business Media LLC, 2021
Erschienen in:Scientific Reports
Sprache:
Englisch
DOI:
10.1038/s41598-021-92159-2
ISSN:
2045-2322
Entstehung:
Anmerkungen:
Beschreibung:
<jats:title>Abstract</jats:title><jats:p>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<jats:italic> Mstn</jats:italic><jats:sup><jats:italic>Ln/Ln</jats:italic></jats:sup> 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.</jats:p>