The DOI matches its Crossref record; 73 of the 74 references it cites were found in a registry or an index.
Skeletal muscle autophagy: a new metabolic regulator
Open accessAbstract
Autophagy classically functions as a physiological process to degrade cytoplasmic components, protein aggregates, and/or organelles, as a mechanism for nutrient breakdown, and as a regulator of cellular architecture. Proper autophagic flux is vital for both functional skeletal muscle, which controls the support and movement of the skeleton, and muscle metabolism. The role of autophagy as a metabolic regulator in muscle has been previously studied; however, the underlying molecular mechanisms that control autophagy in skeletal muscle have only recently begun to emerge. We review recent literature on the molecular pathways controlling skeletal muscle autophagy and discuss how they connect autophagy to metabolic regulation. We also focus on the implications these studies hold for understanding metabolic and muscle-wasting diseases.
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“finely tuned regulation of autophagy is likely necessary for the maintenance of skeletal muscle mass and fitness, as previous studies also suggested that a certain degree of autophagy is necessary to remove damaged proteins and organelles to ensure proper mass and function of skeletal muscle47,52.”
From Disuse-associated loss of the protease Lonp1 in muscle impairs mitochondrial function and causes reduced skeletal muscle mass and strength (2022) · cites this paper as [52]
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RetractedAMPK and mTOR regulate autophagy through direct phosphorylation of Ulk1
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Autophagy in the Pathogenesis of Disease
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Autophagy fights disease through cellular self-digestion
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Autophagy regulates lipid metabolism
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The Beclin 1 network regulates autophagy and apoptosis
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A Narrative Review of Cancer-Related Fatigue (CRF) and Its Possible Pathogenesis
Yang, S., Chu, S., Gao, Y., Ai, Q., Liu, Y., Li, X., & Chen, N. (2019) · Cells · doi:10.3390/cells8070738 · Cited by 242
Liu, C.-C., Lin, Y.-C., Chen, Y.-H., Chen, C.-M., Pang, L.-Y., Chen, H.-A., Wu, P.-R., Lin, M.-Y., Jiang, S.-T., Tsai, T.-F., et al. (2016) · Molecular Cell · doi:10.1016/j.molcel.2015.11.001 · Cited by 215
Self-citationChen, Q., Kirk, K., Shurubor, Y. I., Zhao, D., Arreguin, A. J., Shahi, I., Valsecchi, F., Primiano, G., Calder, E. L., Carelli, V., et al. (2018) · Cell Metabolism · doi:10.1016/j.cmet.2018.03.002 · Cited by 210
Degeneration of Neuromuscular Junction in Age and Dystrophy
Rudolf, R., Khan, M. M., Labeit, S., & Deschenes, M. R. (2014) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2014.00099 · Cited by 197
The ubiquitin proteasome system in atrophying skeletal muscle: roles and regulation
Bilodeau, P., Coyne, E. S., & Wing, S. S. (2016) · American Journal of Physiology-Cell Physiology · doi:10.1152/ajpcell.00125.2016 · Cited by 188
Metadata
- Authors
- Neel, B. A., Lin, Y., & Pessin, J. E.
- Affiliations
- Albert Einstein College of Medicine (US)
- Columbia University (US)
- Corresponding author
- Pessin, Jeffrey E.
- Venue
- Trends in Endocrinology & Metabolism
- Publisher
- Elsevier BV
- Published
- 2013-12
- Volume
- 24
- Issue
- 12
- Pages
- 635-643
- ISSN
- 1043-2760 (ISSN-L)
- PMC
- PMC3849822
- OpenAlex
- W2054835522
- Cited by
- 178
- References
- 74
- Citations by year
- 2026: 9 · 2025: 8 · 2024: 12 · 2023: 7 · 2022: 16 · 2021: 24 · 2020: 20 · 2019: 14 · 2018: 13 · 2017: 16 · 2016: 14 · 2015: 12 · 2014: 13
- FWCI
- 1.54
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Trends in Endocrinology and Metabolism (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health
- National Institute on Aging (AG23475, T32AG023475)
- National Institute of Diabetes and Digestive and Kidney Diseases (R01DK033823, R37DK033823, DK033823, P60DK020541)
- National Institute of Arthritis and Musculoskeletal and Skin Diseases (AR-064420, R01AR064420)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Autophagy in Disease and Therapy
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Muscle Physiology and Disorders
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
- Keywords
- autophagic flux, muscle metabolism, metabolic regulation
- MeSH terms
- Animals, Autophagy, Humans, Signal Transduction, Muscle, Skeletal
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