The DOI matches its Crossref record; 42 of the 42 references it cites were found in a registry or an index.
Role of PGC-1α during acute exercise-induced autophagy and mitophagy in skeletal muscle
Open accessAbstract
Regular exercise leads to systemic metabolic benefits, which require remodeling of energy resources in skeletal muscle. During acute exercise, the increase in energy demands initiate mitochondrial biogenesis, orchestrated by the transcriptional coactivator peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1α). Much less is known about the degradation of mitochondria following exercise, although new evidence implicates a cellular recycling mechanism, autophagy/mitophagy, in exercise-induced adaptations. How mitophagy is activated and what role PGC-1α plays in this process during exercise have yet to be evaluated. Thus we investigated autophagy/mitophagy in muscle immediately following an acute bout of exercise or 90 min following exercise in wild-type (WT) and PGC-1α knockout (KO) animals. Deletion of PGC-1α resulted in a 40% decrease in mitochondrial content, as well as a 25% decline in running performance, which was accompanied by severe acidosis in KO animals, indicating metabolic distress. Exercise induced significant increases in gene transcripts of various mitochondrial (e.g., cytochrome oxidase subunit IV and mitochondrial transcription factor A) and autophagy-related (e.g., p62 and light chain 3) genes in WT, but not KO, animals. Exercise also resulted in enhanced targeting of mitochondria for mitophagy, as well as increased autophagy and mitophagy flux, in WT animals. This effect was attenuated in the absence of PGC-1α. We also identified Niemann-Pick C1, a transmembrane protein involved in lysosomal lipid trafficking, as a target of PGC-1α that is induced with exercise. These results suggest that mitochondrial turnover is increased following exercise and that this effect is at least in part coordinated by PGC-1α. Anna Vainshtein received the AJP-Cell 2015 Paper of the Year award. Listen to a podcast with Anna Vainshtein and coauthor David A. Hood at http://ajpcell.podbean.com/e/ajp-cell-paper-of-the-year-2015-award-podcast/ .
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“explaining the accelerated rate of “re-growth” universally observed in previously trained humans [115,117]”
From Ribosome Biogenesis as a Putative Bottleneck to Skeletal Muscle Hypertrophy: Mechanisms, Human Evidence, and Practical Modulators (2026) · cites this paper as [117]
In the citing paper
“The pre-existing, expanded nucleolar templates are immediately available to rapidly transcribe massive amounts of 45S pre-rRNA”
From Ribosome Biogenesis as a Putative Bottleneck to Skeletal Muscle Hypertrophy: Mechanisms, Human Evidence, and Practical Modulators (2026) · cites this paper as [117]
In the citing paper
“A study conducted on whole-body PGC-1α knockout (KO) and C57BL/6 wild-type (WT) mice subjected to acute physical exercise (run to failure on a treadmill) demonstrated that 90 min postexercise, KO animals presented a 40% reduction in mitochondrial content and a 25% decline in running performance, accompanied by severe lactic acidosis due to reduced aerobic capacity.”
From Exercise-Induced Muscle–Fat Crosstalk: Molecular Mediators and Their Pharmacological Modulation for the Maintenance of Metabolic Flexibility in Aging (2025) · cites this paper as [23]
In the citing paper
“In contrast, WT mice presented an increased expression of mitochondrial biogenesis markers (cytochrome oxidase subunit IV and mitochondrial transcription factor A), as well as autophagy-related factors (p62 and light chain 3) [23].”
From Exercise-Induced Muscle–Fat Crosstalk: Molecular Mediators and Their Pharmacological Modulation for the Maintenance of Metabolic Flexibility in Aging (2025) · cites this paper as [23]
In the citing paper
“PGC-1α activation during physical exercise induces mitochondrial biogenesis, whereas the postexercise recovery phase triggers autophagy and mitophagy to eliminate senescent, dysfunctional, or ROS-damaged mitochondria [23].”
From Exercise-Induced Muscle–Fat Crosstalk: Molecular Mediators and Their Pharmacological Modulation for the Maintenance of Metabolic Flexibility in Aging (2025) · cites this paper as [23]
In the citing paper
“Experimental evidence from PGC-1α knockout mice revealed a sharp decline in mitochondrial content and exercise performance, confirming the importance of this axis in the short-term metabolic remodeling of skeletal muscle [23,33].”
From Exercise-Induced Muscle–Fat Crosstalk: Molecular Mediators and Their Pharmacological Modulation for the Maintenance of Metabolic Flexibility in Aging (2025) · cites this paper as [23]
In the citing paper
“Autophagy induction is not only seen with endurance exercise, but also acute bouts of exercise, and this short-term increase in autophagy appears to require PPARGC1A [488].”
From Autophagy and ALS: mechanistic insights and therapeutic implications (2022) · cites this paper as [488]
In the citing paper
“This outcome is at least partially coordinated by PGC-1α, as the results were not replicated in PGC-1α knockout (KO) mice.”
From Exerkines and Sarcopenia: Unveiling the Mechanism Behind Exercise-Induced Mitochondrial Homeostasis (2025) · cites this paper as [43]
In the citing paper
“acute exercise (90 min) has been observed to result in enhanced mitophagy and an enhanced targeting of mitochondrial degradation, increasing mitochondrial turnover [43].”
From Exerkines and Sarcopenia: Unveiling the Mechanism Behind Exercise-Induced Mitochondrial Homeostasis (2025) · cites this paper as [43]
In the citing paper
“This effect is significantly attenuated in PGC-1α-deficient mice [18].”
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 [18]
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Metadata
- Authors
- Vainshtein, A., Tryon, L. D., Pauly, M., & Hood, D. A.
- Affiliations
- York University (CA)
- Corresponding author
- Hood, David A.
- Venue
- American Journal of Physiology-Cell Physiology
- Publisher
- American Physiological Society
- Published
- 2015-05-01
- Volume
- 308
- Issue
- 9
- Pages
- C710-C719
- ISSN
- 0363-6143 (ISSN-L)
- 1522-1563
- PMC
- PMC4420796
- OpenAlex
- W2057731584
- Cited by
- 273
- References
- 42
- Citations by year
- 2026: 19 · 2025: 21 · 2024: 17 · 2023: 18 · 2022: 27 · 2021: 29 · 2020: 30 · 2019: 32 · 2018: 35 · 2017: 25 · 2016: 14 · 2015: 6
- FWCI
- 20.92
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- American Journal of Physiology-Cell Physiology (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Gouvernement du Canada | Natural Sciences and Engineering Research Council of Canada (Conseil de Recherches en Sciences Naturelles et en Génie du Canada)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Autophagy in Disease and Therapy
- Health Sciences › Medicine › Physiology (medical) › Adipose Tissue and Metabolism
- Health Sciences › Medicine › Physiology (medical) › Exercise and Physiological Responses
- Keywords
- PGC-1α, acute exercise, autophagy, mitophagy, skeletal muscle, mitochondrial biogenesis, mitochondrial turnover, Niemann-Pick C1, exercise-induced acidosis, running performance, p62, TFAM
- MeSH terms
- Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha, Forkhead Box Protein O3, Niemann-Pick C1 Protein, Acidosis, Animals, Autophagy, Physical Exertion, Gene Expression Regulation, Mice, Inbred C57BL, Mitochondria, Muscle, Muscle Contraction, Proteins, RNA, Messenger, Time Factors, Transcription Factors, Signal Transduction, Biomarkers, Mice, Knockout, Muscle, Skeletal, Lactic Acid, Intracellular Signaling Peptides and Proteins, Basic Helix-Loop-Helix Leucine Zipper Transcription Factors, Forkhead Transcription Factors, Mitophagy
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