Regulation of Myostatin on the Growth and Development of Skeletal Muscle

Abstract

Myostatin (MSTN), a member of the transforming growth factor-β superfamily, can negatively regulate the growth and development of skeletal muscle by autocrine or paracrine signaling. Mutation of the myostatin gene under artificial or natural conditions can lead to a significant increase in muscle quality and produce a double-muscle phenotype. Here, we review the similarities and differences between myostatin and other members of the transforming growth factor-β superfamily and the mechanisms of myostatin self-regulation. In addition, we focus extensively on the regulation of myostatin functions involved in myogenic differentiation, myofiber type conversion, and skeletal muscle protein synthesis and degradation. Also, we summarize the induction of reactive oxygen species generation and oxidative stress by myostatin in skeletal muscle. This review of recent insights into the function of myostatin will provide reference information for future studies of myostatin-regulated skeletal muscle formation and may have relevance to agricultural fields of study.

Muscle Wasting in Chronic Kidney Disease: Mechanism and Clinical Implications—A Narrative Review

“…On the other hand, the myostatin signaling pathway is a critical negative regulator of skeletal muscle mass, which is upregulated in skeletal muscle of patients with CKD [ 41 ] in response to oxidative stress, inflammation, uremic toxins, angiotensin II, glucocorticoids, and metabolic acidosis in CKD [ 26 , 42 ]. Myostatin or growth development factor-8 (GDF-8) is a member of the transforming growth factor-β (TGF-β) superfamily and is secreted by mature muscle cells [ 43 ]. The role of myostatin in muscle wasting during CKD involves UPS activation and inhibition of muscle satellite cell recruitment [ 26 ].…”

NADPH Oxidases Connecting Fatty Liver Disease, Insulin Resistance and Type 2 Diabetes: Current Knowledge and Therapeutic Outlook

“…From a clinical perspective, circulating MSTN levels are elevated in individuals with obesity, and weight loss reduces MSTN levels and improves insulin sensitivity [ 193 , 194 ]. Myostatin can activate ROS production by a yet undetermined NOX enzyme isoform in muscle cells, although similar activity in hepatocytes has not yet been reported [ 195 ]. Irisin exerts a positive effect on hepatocyte lipid metabolism by inhibiting the lipogenic regulators LXRα and SREBP1c and suppressing inflammatory cytokine production through NF-κB [ 196 ].…”

Organokines in Rheumatoid Arthritis: A Critical Review

“…RF and ACPA are the most studied molecules studied in RA patients. However, ACPA seems to be more specific than RF in the pathogenesis of the disease due to the ability of citrullinated auto-antibodies to target citrullinated proteins and form with these proteins the structures called immune complexes, which are accumulated in the synovial fluid [ 7 , 33 , 34 ].…”

“…This myokine affects fat and glucose metabolisms, affecting adipocyte proliferation and cardiomyocyte homeostasis. Additionally, myostatin also influences bone homeostasis and is associated with bone development [ 34 , 38 ].…”

“…Remembering myostatin’s physiological roles and combining it to the elevated serum levels among RA individuals, myostatin in RA increases muscle atrophy and osteoclasts differentiation, promoting muscle degradation and bone destruction. This myokine can also stimulate Th-17 cells migration to the inflamed RA joints through the mechanism derived from the myostatin-CCL20-CCR6 axis [ 19 , 34 , 38 , 39 , 40 , 41 , 42 , 43 ].…”