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 LabeitPublished 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.