ArticleProceedings of the National Academy of Sciences of the United States of America2013
The transcriptional coactivator PGC-1α is dispensable for chronic overload-induced skeletal muscle hypertrophy and metabolic remodeling.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed.
- Skeletal Muscle PGC-1α Remodels Mitochondrial Phospholipidome but Does Not Alter Energy Efficiency for ATP Synthesis.Journal of cachexia, sarcopenia and muscle · 2025Article
- Mechanisms of mechanical overload-induced skeletal muscle hypertrophy: current understanding and future directions.Physiological reviews · 2023Review
- RNA-bound PGC-1α controls gene expression in liquid-like nuclear condensates.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Advantages of targeting the tumor immune microenvironment over blocking immune checkpoint in cancer immunotherapy.Signal transduction and targeted therapy · 2021Review
- Molecular Mechanisms of Skeletal Muscle Hypertrophy.Journal of neuromuscular diseases · 2021Review
- Muscle hypertrophy and muscle strength: dependent or independent variables? A provocative review.European journal of translational myology · 2020Article
- p38 MAPK in Glucose Metabolism of Skeletal Muscle: Beneficial or Harmful?International journal of molecular sciences · 2020Review
- βExperimental neurology · 2019Article
- Deficiency ofFrontiers in sports and active living · 2019Article
- Increased FXYD1 and PGC-1α mRNA after blood flow-restricted running is related to fibre type-specific AMPK signalling and oxidative stress in human muscle.Acta physiologica (Oxford, England) · 2018Article
- PGC-1α affects aging-related changes in muscle and motor function by modulating specific exercise-mediated changes in old mice.Aging cell · 2018Article
- Moderate Modulation of Cardiac PGC-1α Expression Partially Affects Age-Associated Transcriptional Remodeling of the Heart.Frontiers in physiology · 2018Article
- Overload-mediated skeletal muscle hypertrophy is not impaired by loss of myofiber STAT3.American journal of physiology. Cell physiology · 2017Article
- Exploring the Role of PGC-1α in Defining Nuclear Organisation in Skeletal Muscle Fibres.Journal of cellular physiology · 2017Article
- Muscle PGC-1α modulates satellite cell number and proliferation by remodeling the stem cell niche.Skeletal muscle · 2016Article
- The Genomic Context and Corecruitment of SP1 Affect ERRα Coactivation by PGC-1α in Muscle Cells.Molecular endocrinology (Baltimore, Md.) · 2016Article
- Skeletal muscle PGC-1α modulates systemic ketone body homeostasis and ameliorates diabetic hyperketonemia in mice.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2016Article
- AMPKγ3 is dispensable for skeletal muscle hypertrophy induced by functional overload.American journal of physiology. Endocrinology and metabolism · 2016Article
- PGC-1α modulates necrosis, inflammatory response, and fibrotic tissue formation in injured skeletal muscle.Skeletal muscle · 2016Article
- The hitchhiker's guide to PGC-1α isoform structure and biological functions.Diabetologia · 2015Review
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Authors and funding
5 authors.
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Abstract
Skeletal muscle mass loss and dysfunction have been linked to many diseases. Conversely, resistance exercise, mainly by activating mammalian target of rapamycin complex 1 (mTORC1), promotes skeletal muscle hypertrophy and exerts several therapeutic effects. Moreover, mTORC1, along with peroxisome proliferator-activated receptor γ coactivator 1α (PGC-1α), regulates skeletal muscle metabolism. However, it is unclear whether PGC-1α is required for skeletal muscle adaptations after overload. Here we show that although chronic overload of skeletal muscle via synergist ablation (SA) strongly induces hypertrophy and a switch toward a slow-contractile phenotype, these effects were independent of PGC-1α. In fact, SA down-regulated PGC-1α expression and led to a repression of energy metabolism. Interestingly, however, PGC-1α deletion preserved peak force after SA. Taken together, our data suggest that PGC-1α is not involved in skeletal muscle remodeling induced by SA.
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