RAGE in the pathophysiology of skeletal muscle

J Cachexia Sarcopenia Muscle. 2018 Dec;9(7):1213-1234. doi: 10.1002/jcsm.12350. Epub 2018 Oct 18.

Abstract

Emerging evidence suggests that the signalling of the Receptor for Advanced Glycation End products (RAGE) is critical for skeletal muscle physiology controlling both the activity of muscle precursors during skeletal muscle development and the correct time of muscle regeneration after acute injury. On the other hand, the aberrant re-expression/activity of RAGE in adult skeletal muscle is a hallmark of muscle wasting that occurs in response to ageing, genetic disorders, inflammatory conditions, cancer, and metabolic alterations. In this review, we discuss the mechanisms of action and the ligands of RAGE involved in myoblast differentiation, muscle regeneration, and muscle pathological conditions. We highlight potential therapeutic strategies for targeting RAGE to improve skeletal muscle function.

Keywords: AGEs; HMGB1; RAGE; S100B; muscle wasting; myogenesis.

Publication types

  • Review

MeSH terms

  • Animals
  • Gene Expression Regulation
  • Humans
  • Ligands
  • Muscle, Skeletal / metabolism*
  • Muscle, Skeletal / pathology
  • Muscular Atrophy / etiology
  • Muscular Atrophy / metabolism
  • Muscular Atrophy / pathology
  • Muscular Diseases / etiology*
  • Muscular Diseases / metabolism*
  • Muscular Diseases / pathology
  • Protein Isoforms
  • Receptor for Advanced Glycation End Products / antagonists & inhibitors
  • Receptor for Advanced Glycation End Products / chemistry
  • Receptor for Advanced Glycation End Products / genetics
  • Receptor for Advanced Glycation End Products / metabolism*
  • Rhabdomyosarcoma / etiology
  • Rhabdomyosarcoma / metabolism
  • Rhabdomyosarcoma / pathology
  • Signal Transduction

Substances

  • Ligands
  • Protein Isoforms
  • Receptor for Advanced Glycation End Products