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In their article, Biesemann et al1 extensively characterized the molecular and functional changes resulting from selective deletion of myostatin in adult cardiomyocytes using a tamoxifen inducible Cre transgenic mouse model. With this model, loss of myostatin in cardiomyocytes leads to a spontaneous cardiomyopathy phenotype and ≈30% mortality within 10 days of starting tamoxifen treatment, although surviving mice eventually regained normal heart function.Loss of skeletal muscle mass, sarcopenia, has emerged as a critical determinant of the clinical outcomes in aging, heart failure, and cancer. Myostatin inhibition is considered to be a potential therapeutic strategy for sarcopenia because of its role as a negative regulator of muscle mass.2,3 Constitutive loss of cardiomyocyte-derived myostatin in mice starting in early embryonic development does not lead to aggravated cardiac pathology, but it does rescue skeletal muscle atrophy in pressure overload–induced heart failure.2 However, a recent study found that plasma levels of the myostatin prodomain were actually reduced in patients with heart failure compared with healthy controls,4 although these patients were not cachexic and muscle mass was not assessed; so it is still possible that a heart failure patient cohort with confirmed sarcopenia may have elevated plasma myostatin. The pathological consequences of myostatin deletion in the heart presented by Biesemann et al1 pose a serious deterrent to the use …

Letter by McLean and Oudit Regarding Article, “Myostatin Regulates Energy Homeostasis in the Heart and Prevents Heart Failure”