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Targeting MuRF1 by small molecules in a HFpEF rat model improves myocardial diastolic function and skeletal muscle contractility.

Volker AdamsAntje SchauerAntje AugsteinVirginia KirchhoffRuna DraskowskiAnett JannaschKeita GotoGemma LyallAnita MännelPeggy BarthelNorman MangnerEphraim B WinzerAxel LinkeSiegfried Labeit
Published in: Journal of cachexia, sarcopenia and muscle (2022)
MyoMed-205 improved myocardial diastolic function and prevented SKM atrophy/function in the ZSF1 animal model of HFpEF. Mechanistically, SKM benefited from an attenuated ubiquitin proteasome system and augmented synthesis/activity of proteins of the mitochondrial respiratory chain while the myocardium seemed to benefit from reduced titin modifications and fibrosis.
Keyphrases
  • left ventricular
  • skeletal muscle
  • blood pressure
  • heart failure
  • small molecule
  • type diabetes
  • cancer therapy
  • respiratory tract
  • liver fibrosis