PGC-1α modulates denervation-induced mitophagy in skeletal muscle
Open accessAbstract
BACKGROUND: Alterations in skeletal muscle contractile activity necessitate an efficient remodeling mechanism. In particular, mitochondrial turnover is essential for tissue homeostasis during muscle adaptations to chronic use and disuse. While mitochondrial biogenesis appears to be largely governed by the transcriptional co-activator peroxisome proliferator co-activator 1 alpha (PGC-1α), selective mitochondrial autophagy (mitophagy) is thought to mediate organelle degradation. However, whether PGC-1α plays a direct role in autophagy is currently unclear. METHODS: To investigate the role of the co-activator in autophagy and mitophagy during skeletal muscle remodeling, PGC-1α knockout (KO) and overexpressing (Tg) animals were unilaterally denervated, a common model of chronic muscle disuse. RESULTS: Animals lacking PGC-1α exhibited diminished mitochondrial density alongside myopathic characteristics reminiscent of autophagy-deficient muscle. Denervation promoted an induction in autophagy and lysosomal protein expression in wild-type (WT) animals, which was partially attenuated in KO animals, resulting in reduced autophagy and mitophagy flux. PGC-1α overexpression led to an increase in lysosomal capacity as well as indicators of autophagy flux but exhibited reduced localization of LC3II and p62 to mitochondria, compared to WT animals. A correlation was observed between the levels of the autophagy-lysosome master regulator transcription factor EB (TFEB) and PGC-1α in muscle, supporting their coordinated regulation. CONCLUSIONS: Our investigation has uncovered a regulatory role for PGC-1α in mitochondrial turnover, not only through biogenesis but also via degradation using the autophagy-lysosome machinery. This implies a PGC-1α-mediated cross-talk between these two opposing processes, working to ensure mitochondrial homeostasis during muscle adaptation to chronic disuse.
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PPARGC1A plays a role in activating the autophagy-lysosome pathway and specifically mitophagy in muscle.
“More recently, it has been shown that PPARGC1A also plays a role in activating the autophagy‐lysosome pathway (Takikita et al., 2010) and specifically mitophagy in muscle (Vainshtein et al., 2015).”
From Autophagy gene expression in skeletal muscle of older individuals is associated with physical performance, muscle volume and mitochondrial function in the study of muscle, mobility and aging ( <scp>SOMMA</scp> ) (2024) · cites this paper as Vainshtein et al., 2015
The Conclusions report that PGC-1α regulates mitophagy in skeletal muscle, and the Discussion says physiological levels are required for its proper propagation. But the Conclusions also report that PGC-1α overexpression suppresses mitophagy, so describing its role simply as activating mitophagy overstates the finding. The autophagy-lysosome pathway portion of the citing sentence is attributed to Takikita et al., not to this source. (LLM, conf=0.87)
Experimental — accuracy not yet measuredExcessive activation of autophagy aggravates muscle wasting by removing portion of cytoplasm, proteins, and organelles.
“Excessive activation of autophagy aggravates muscle wasting by removing portion of cytoplasm, proteins, and organelles30,50,51”
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 [51]
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“More recently, it has been shown that PPARGC1A also plays a role in activating the autophagy-lysosome pathway (Takikita et al., 2010 ) and specifically mitophagy in muscle (Vainshtein et al., 2015 ).”
- Authors
- Vainshtein, A., Desjardins, E. M., Armani, A., Sandri, M., & Hood, D. A.
- Affiliations
- York University (CA)
- University of Padua (IT)
- Corresponding author
- Hood, David A
- Venue
- Skeletal Muscle
- Published
- 2015-03-18
- Volume
- 5
- Issue
- 1
- Pages
- 9-9
- ISSN
- 2044-5040 (ISSN-L)
- PMC
- PMC4381453
- OpenAlex
- W2112956181
- Cited by
- 181
- References
- 53
- Citations by year
- 2026: 13 · 2025: 13 · 2024: 15 · 2023: 11 · 2022: 12 · 2021: 25 · 2020: 14 · 2019: 16 · 2018: 23 · 2017: 11 · 2016: 18 · 2015: 10
- FWCI
- 16.20
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Skeletal Muscle (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Funders
- Natural Sciences and Engineering Research Council of Canada
- Topics
- Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Muscle Physiology and Disorders
- Health Sciences › Medicine › Physiology › Adipose Tissue and Metabolism
- Keywords
- PGC-1α, mitophagy, muscle denervation, mitochondrial turnover, autophagy-lysosome pathway, mitochondrial biogenesis, TFEB, lysosomal proteins, LC3-II, p62, mitochondrial homeostasis, muscle atrophy
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