Key result
Cardiac myostatin inhibition prevents skeletal muscle wasting in experimental heart failure.
Why the study?
The cause of skeletal muscle wasting and cachexia in heart failure remains unknown, with a hypothesis that cardiac myostatin secretion promotes systemic muscle atrophy.
Does targeted inhibition or genetic deletion of myostatin prevent skeletal muscle atrophy in heart failure?
Does targeted inhibition or genetic deletion of myostatin prevent skeletal muscle atrophy in heart failure?
Myostatin released from cardiomyocytes drives skeletal muscle wasting in heart failure, suggesting myostatin inhibition as a potential therapy for cardiac cachexia.
No takes yet. Share an insight, caveat, or question.
Should not yet inform HF cachexia management; leaves open myostatin inhibition for human trials.
Heineke et al. (2010) studied Cardiac cachexia and heart failure. Heart-specific deletion of myostatin (Mstn) or myostatin blocking antibody (JA-16) vs. Wild-type mice was evaluated on Skeletal muscle wasting and atrophy. Heart-specific deletion of myostatin or infusion of a myostatin blocking antibody prevented skeletal muscle wasting in mice with pressure overload-induced heart failure.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: