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2016 ; 19
(3
): 177-81
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Neuromuscular junction degeneration in muscle wasting
#MMPMID26870889
Rudolf R
; Deschenes MR
; Sandri M
Curr Opin Clin Nutr Metab Care
2016[May]; 19
(3
): 177-81
PMID26870889
show ga
PURPOSE OF REVIEW: Denervation is a hallmark of age-related and other types of
muscle wasting. This review focuses on recent insights and current viewpoints
regarding the mechanisms and clinical relevance of maintaining the neuromuscular
junction to counteract muscle wasting resulting from aging or neural
disease/damage. RECENT FINDINGS: Activity-dependent regulation of autophagy, the
agrin-muscle specific kinase-Lrp4 signaling axis, and sympathetic modulation are
principal mechanisms involved in stabilizing the neuromuscular junction. These
findings are derived from several animal models and were largely confirmed by
human gene expression analysis as well as insights from rare neuromuscular
diseases such as amyotrophic lateral sclerosis and congenital myasthenic
syndromes. Based on these insights, agrin-derived fragments are currently being
evaluated as biomarkers for age-related muscle wasting. Tuning of autophagy, of
the agrin pathway, and of sympathetic input are being studied as clinical
treatment of muscle wasting disorders. SUMMARY: Basic research has revealed that
maintenance of neuromuscular junctions and a few signaling pathways are important
in the context of age-dependent and other forms of muscle wasting. These findings
have recently started to enter clinical practice, but further research needs to
substantiate and refine our knowledge.
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