ArticleThe Journal of physiology2014
PGC1-α over-expression prevents metabolic alterations and soleus muscle atrophy in hindlimb unloaded mice.
Article in The Journal of physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 131 papers.
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Who cites it
131 citing papers in PubMed, 220 citations in OpenAlex.
- Supplementation with a Bioactive Melon Concentrate in Humans and Animals: Prevention of Oxidative Damages and Fatigue in the Context of a Moderate or Eccentric Physical Activity.International journal of environmental research and public health · 2020Trial
- PlanHabThe Journal of physiology · 2018Trial
- Plant‑derived natural products alleviate dexamethasone‑induced skeletal muscle atrophy by modulating FoxO (Review).International journal of molecular medicine · 2026Review
- Exercise-induced modulation of the unfolded protein response: a therapeutic avenue for muscle wasting disorders.Journal of physiology and biochemistry · 2026Review
- Impact of mechanical unloading on the irisin precursor, FNDC5, in skeletal muscle of sheep as a large animal experimental model.JBMR plus · 2026Article
- Physical exercise protects against Toxoplasma gondii infection-induced muscle atrophy and microvascular rarefaction.Communications biology · 2026Article
- Dihydropyridine Receptor Inhibition Attenuates Force and Fiber Cross-Sectional Area Decrease in the Three-Day Unloaded Rat Soleus Muscle.International journal of molecular sciences · 2026Article
- Intermittent fasting and neuroprotection in Alzheimer's disease: metabolic mechanisms, cellular signaling, and brain-peripheral crosstalk.Frontiers in nutrition · 2026Review
- Autophagy selectively clears ER in TNF-α-induced muscle atrophy.Autophagy reports · 2026Article
- PGC-1α: key regulator of mitochondrial biogenesis and cellular differentiation in metabolic and regenerative tissues.Cell & bioscience · 2025Review
- Disuse-induced muscle-type specific alterations and adiponectin pathway response in male mice.Physiological reports · 2025Article
- Residual force enhancement following hindlimb unloading and exercise prehabilitation.Journal of muscle research and cell motility · 2025Article
- Acupuncture treatment preserves soleus muscle mass and improves mitochondrial function in a rat model of disuse atrophy.Integrative medicine research · 2025Article
- A new Drosophila model of prolonged inactivity shortens lifespan and impairs muscle function.Scientific reports · 2025Article
- Resistance and Aerobic Preconditioning Delays Unloading-Induced Multisystemic Physiological Changes: The NEBULA Project.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Aging and Altered Gravity: A Cellular Perspective.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Review
- Dietary nitrate preserves mitochondrial bioenergetics and mitochondrial protein synthesis rates during short-term immobilization in mice.The Journal of physiology · 2025Article
- Metabolic dysregulation contributes to the development of dysferlinopathy.Life science alliance · 2025Article
- DNA hypermethylation preceded by H3K27 trimethylation is linked to downregulation of gene expression in disuse muscle atrophy in male mice.Physiological reports · 2025Article
- Resistance but not endurance training suppresses glucocorticoid-induced leucine zipper (GILZ) expression in human skeletal muscle.European journal of applied physiology · 2025Article
71 more citing papers are in PubMed but not listed here.
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5 authors at 2 institutions in 1 country.
Funding
Abstract
Prolonged skeletal muscle inactivity causes muscle fibre atrophy. Redox imbalance has been considered one of the major triggers of skeletal muscle disuse atrophy, but whether redox imbalance is actually the major cause or simply a consequence of muscle disuse remains of debate. Here we hypothesized that a metabolic stress mediated by PGC-1α down-regulation plays a major role in disuse atrophy. First we studied the adaptations of soleus to mice hindlimb unloading (HU) in the early phase of disuse (3 and 7 days of HU) with and without antioxidant treatment (trolox). HU caused a reduction in cross-sectional area, redox status alteration (NRF2, SOD1 and catalase up-regulation), and induction of the ubiquitin proteasome system (MuRF-1 and atrogin-1 mRNA up-regulation) and autophagy (Beclin1 and p62 mRNA up-regulation). Trolox completely prevented the induction of NRF2, SOD1 and catalase mRNAs, but not atrophy or induction of catabolic systems in unloaded muscles, suggesting that oxidative stress is not a major cause of disuse atrophy. HU mice showed a marked alteration of oxidative metabolism. PGC-1α and mitochondrial complexes were down-regulated and DRP1 was up-regulated. To define the link between mitochondrial dysfunction and disuse muscle atrophy we unloaded mice overexpressing PGC-1α. Transgenic PGC-1α animals did not show metabolic alteration during unloading, preserving muscle size through the reduction of autophagy and proteasome degradation. Our results indicate that mitochondrial dysfunction plays a major role in disuse atrophy and that compounds inducing PGC-1α expression could be useful to treat/prevent muscle atrophy.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.