Epigenetics of Skeletal Muscle Atrophy

Abstract

Skeletal muscle atrophy, characterized by diminished muscle strength and mass, arises from various causes, including malnutrition, aging, nerve damage, and disease-related secondary atrophy. Aging markedly escalates the prevalence of sarcopenia. Concurrently, the incidence of muscle atrophy significantly rises among patients with chronic ailments such as heart failure, diabetes, and chronic obstructive pulmonary disease (COPD). Epigenetics plays a pivotal role in skeletal muscle atrophy. Aging elevates methylation levels in the promoter regions of specific genes within muscle tissues. This aberrant methylation is similarly observed in conditions like diabetes, neurological disorders, and cardiovascular diseases. This study aims to explore the relationship between epigenetics and skeletal muscle atrophy, thereby enhancing the understanding of its pathogenesis and uncovering novel therapeutic strategies.

Keywords: epigenetics; skeletal muscle atrophy.

Figure 1

The pathogenesis of skeletal muscle atrophy. Skeletal muscle atrophy is often accompanied by activation of the UPS system, impaired autophagic flux, decreased protein synthesis, and elevated levels of oxidative stress, inflammation, caspases and calpain.

Figure 2

The pathway related to skeletal muscle atrophy. PI3K/AKT, NF-κB, AMPK and myostatin pathways play an important role in muscular atrophy. The PI3K/AKT pathway can promote protein synthesis, inhibit the UPS system and improve autophagy flux. The NF-κB pathway can promote inflammation and the UPS system. AMPK is more responsible, it can inhibit mTOR but promote PGC1α. Myostatin can affect the UPS system through the Smad pathway.