Myostatin in Aging and Disease

Dear Colleagues,

Myostatin, also known as growth and differentiation factor 8 (GDF8), is a member of the transforming growth factor β (TGF‐β) superfamily. Myostatin is primarily expressed in skeletal muscle, where it acts as a negative regulator of muscle growth and development, and has long been linked to muscle wasting disorders. Much work has elucidated downstream signalling following the binding of activated myostatin to the activin type II receptor to effect change in muscle size, in addition to metabolic adaptations. Given the prominent role for myostatin in the regulation of muscle size, as well its impact on metabolism and function of neighbouring tissues, myostatin shows great promise as a therapeutic target. Elevations in myostatin expression have been suggested to participate in muscle wasting during disuse, cancer, ageing, liver disease, end stage renal disease, COPD, and numerous other acute and chronic catabolic conditions. However, recent results from clinical trials of myostatin inhibitors have somewhat challenged the early promise of myostatin inhibition-based therapies. More recent work has also begun to dissect many of the molecular mechanisms whereby myostatin alters neighbouring tissues as a myokine. These include but are not limited to osteoblastic differentiation, obesity development, insulin resistance, fibrotic processes, and local and systemic inflammation. For these reasons, a greater understanding of myostatin induction, regulation, and overall function is needed to dissect and validate myostatin as a prognostic biomarker and therapeutic target for treating muscle and metabolic diseases. This Special Issue of Cells will improve our understanding of how myostatin contributes to skeletal muscle metabolism; ageing; and, ultimately, disease pathology. Given the conservation of the myostatin gene across several animal species, including vertebrate and invertebrate, submissions are welcome from those studying model organisms.

We are looking forward to your contributions to this Special Issue.

Dr. Christopher Fry
Guest Editor

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• regulation of gene expression
• skeletal muscle atrophy and catabolism
• cellular signaling transduction
• insulin resistance and metabolic imbalance
• bone formation