Skeletal muscle autophagy and its role in sarcopenia and organismal aging

Jiao, Jianqin; Demontis, Fabio

doi:10.1016/j.coph.2017.03.009

Cited by 184Muscle Physiology and DisordersAutophagy in Disease and TherapyNutrition and Health in Aging

Skeletal muscle autophagy and its role in sarcopenia and organismal aging

Jiao, Jianqin, Demontis, Fabio·2017·Current Opinion in Pharmacology

DOI 10.1016/j.coph.2017.03.009

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Abstract

Sarcopenia, the loss of skeletal muscle mass and strength in the aged, is an important medical condition but its etiology is incompletely understood. Because autophagy promotes myofiber atrophy in the young, it was believed that autophagy inhibition would prevent sarcopenia. However, recent studies have revealed that autophagy actually maintains muscle mass and that its function declines during muscle aging. Consistently, boosting basal autophagy protects from age-related muscle dysfunction by promoting the selective degradation of misfolded proteins and dysfunctional organelles. Conversely, autophagy inhibition leads to loss of muscle strength and induces a maladaptive stress response responsible for myofiber atrophy in the aged. In addition to cell-autonomous effects, muscle autophagy and associated signaling pathways induce systemic responses in other aging tissues by modulating the expression and secretion of myokines. We propose that myokines and pharmacologic interventions that boost selective autophagy may prevent sarcopenia, delay systemic aging, and extend health span.

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Imbalance of protein synthesis and protein degradation during aging can lead to declined mass of skeletal muscle, common in senile muscular atrophy.
“Increasing evidence has demonstrated that the imbalance of protein synthesis and protein degradation during the aging process can lead to the declined mass of skeletal muscle, a common occurrence in senile muscular atrophy [27].”
From Lifelong Aerobic Exercise Alleviates Sarcopenia by Activating Autophagy and Inhibiting Protein Degradation via the AMPK/PGC-1α Signaling Pathway (2021) · cites this paper as [27]

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Authors: Jiao, J., & Demontis, F.
Affiliations: St. Jude Children's Research Hospital (US)
Corresponding author: Demontis, Fabio
ORCID: Demontis, Fabio
Venue: Current Opinion in Pharmacology
Publisher: Elsevier BV
Published: 2017-06
Volume: 34
Pages: 1-6
ISSN: 1471-4892 (ISSN-L)
DOI: 10.1016/j.coph.2017.03.009
OpenAlex: W2605686103
Cited by: 184
References: 56
Citations by year: 2026: 15 · 2025: 15 · 2024: 25 · 2023: 22 · 2022: 22 · 2021: 29 · 2020: 24 · 2019: 21 · 2018: 6 · 2017: 5
FWCI: 1.43
Type: journal article
Language: en
Open access: closed
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations: Current Opinion in Pharmacology (publishedVersion)
PubMed (publishedVersion)
Funders: Ellison Medical Foundation
American Federation for Aging Research
Glenn Foundation for Medical Research, the Hartwell Foundation
American Parkinson Disease Association
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Muscle Physiology and Disorders
Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
Health Sciences › Medicine › Physiology › Nutrition and Health in Aging
Keywords: sarcopenia, biological aging, muscle fiber atrophy, selective autophagy, myokines, misfolded protein degradation, healthspan, autophagy inhibition
MeSH terms: Aging, Animals, Autophagy, Humans, Muscle, Skeletal, Intercellular Signaling Peptides and Proteins, Sarcopenia

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Skeletal muscle autophagy and its role in sarcopenia and organismal aging

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