Metabolic Pathways and Ion Channels Involved in Skeletal Muscle Atrophy: A Starting Point for Potential Therapeutic Strategies

Cells. 2022 Aug 18;11(16):2566. doi: 10.3390/cells11162566.

Abstract

Skeletal muscle tissue has the important function of supporting and defending the organism. It is the largest apparatus in the human body, and its function is important for contraction and movements. In addition, it is involved in the regulation of protein synthesis and degradation. In fact, inhibition of protein synthesis and/or activation of catabolism determines a pathological condition called muscle atrophy. Muscle atrophy is a reduction in muscle mass resulting in a partial or complete loss of function. It has been established that many physiopathological conditions can cause a reduction in muscle mass. Nevertheless, it is not well known the molecular mechanisms and signaling processes causing this dramatic event. There are multiple concomitant processes involved in muscle atrophy. In fact, the gene transcription of some factors, oxidative stress mechanisms, and the alteration of ion transport through specific ion channels may contribute to muscle function impairment. In this review, we focused on the molecular mechanisms responsible for muscle damage and potential drugs to be used to alleviate this disabling condition.

Keywords: atrophy; disuse; hindlimb unloading; ion channels; sarcopenia; skeletal muscle.

Publication types

  • Review

MeSH terms

  • Hindlimb Suspension* / physiology
  • Humans
  • Ion Channels / metabolism
  • Metabolic Networks and Pathways
  • Muscle, Skeletal / metabolism
  • Muscular Atrophy* / pathology

Substances

  • Ion Channels

Grants and funding

This research received no external funding.