ArticleThe Journal of physiology2013
Acute exercise induces tumour suppressor protein p53 translocation to the mitochondria and promotes a p53-Tfam-mitochondrial DNA complex in skeletal muscle.
Article in The Journal of physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 papers, 1 of them a synthesis that pooled it.
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Who cites it
79 citing papers in PubMed, 1 synthesis or guideline pooled it, 137 citations in OpenAlex.
- A systematic review of p53 regulation of oxidative stress in skeletal muscle.Redox report : communications in free radical research · 2018Pooled it
- Skeletal Muscle MicroRNA Patterns in Response to a Single Bout of Exercise in Females: Biomarkers for Subsequent Training Adaptation?Biomolecules · 2023Trial
- Metabolic stress-dependent regulation of the mitochondrial biogenic molecular response to high-intensity exercise in human skeletal muscle.The Journal of physiology · 2018Trial
- Polyphenol supplementation alters intramuscular apoptotic signaling following acute resistance exercise.Physiological reports · 2018Trial
- Sprint-interval training with post-exercise blood flow restriction increases mitochondrial content and respiration.The Journal of physiology · 2026Article
- Reactive oxygen species in health and disease.Molecular biomedicine · 2026Review
- Mitochondrial transcription factor A: linking mtDNA maintenance, mitochondrial stress responses, and inflammaging.Frontiers in aging · 2026Review
- Adaptations in mitochondrial quality control and interactions with innate immune signaling within skeletal muscle: A narrative review.Journal of sport and health science · 2025Review
- The Influence of an Acute Endurance Intervention on Breast Cancer Cell Growth-A Pilot Study.International journal of molecular sciences · 2025Article
- Mitochondrial Biogenesis in Skeletal Muscle.Advances in experimental medicine and biology · 2025Review
- Skeletal muscle p53-depletion uncovers a mechanism of fuel usage suppression that enables efficient energy conservation.Journal of cachexia, sarcopenia and muscle · 2024Article
- RORα-GABP-TFAM axis alleviates myosteatosis with fatty atrophy through reinforcement of mitochondrial capacity.Journal of cachexia, sarcopenia and muscle · 2024Article
- The Acute, Short-, and Long-Term Effects of Endurance Exercise on Skeletal Muscle Transcriptome Profiles.International journal of molecular sciences · 2024Article
- Glyoxalase I is a novel target for the prevention of metabolic derangement.Pharmacology & therapeutics · 2023Review
- Exercise metabolism and adaptation in skeletal muscle.Nature reviews. Molecular cell biology · 2023Review
- High-Intensity Interval Training Improves Glycemic Control, Cellular Apoptosis, and Oxidative Stress of Type 2 Diabetic Patients.Medicina (Kaunas, Lithuania) · 2023Article
- Drp1/p53 interaction mediates p53 mitochondrial localization and dysfunction in septic cardiomyopathy.Journal of molecular and cellular cardiology · 2023Article
- Advances in exercise to alleviate sarcopenia in older adults by improving mitochondrial dysfunction.Frontiers in physiology · 2023Review
- Mitochondrial epigenetics in aging and cardiovascular diseases.Frontiers in cardiovascular medicine · 2023Review
- Long non-coding RNA Tug1 modulates mitochondrial and myogenic responses to exercise in skeletal muscle.BMC biology · 2022Article
19 more citing papers are in PubMed but not listed here.
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The major tumour suppressor protein p53 plays an important role in maintaining mitochondrial content and function in skeletal muscle. p53 has been shown to reside in the mitochondria complexed with mitochondrial DNA (mtDNA); however, the physiological repercussions of mitochondrial p53 remain unknown. We endeavoured to elucidate whether an acute bout of endurance exercise could mediate an increase in mitochondrial p53 levels. C57Bl6 mice (n = 6 per group) were randomly assigned to sedentary, acute exercise (AE, 15 m min(-1) for 90 min) or acute exercise + 3 h recovery (AER) groups. Exercise concomitantly increased the mRNA content of nuclear-encoded (PGC-1α, Tfam, NRF-1, COX-IV, citrate synthase) and mtDNA-encoded (COX-I) genes in the AE group, and further by ∼5-fold in the AER group. Nuclear p53 protein levels were reduced in the AE and AER groups, while in contrast, the abundance of p53 was drastically enhanced by ∼2.4-fold and ∼3.9-fold in subsarcolemmal and intermyofibrillar mitochondria, respectively, in the AER conditions. Within the mitochondria, the interaction of p53 with mtDNA at the D-loop and with Tfam was elevated by ∼4.6-fold and ∼3.6-fold, respectively, in the AER group. In the absence of p53, the enhanced COX-I mRNA content observed with AE and AER was abrogated. This study is the first to indicate that endurance exercise can signal to localize p53 to the mitochondria where it may serve to positively modulate the activity of the mitochondrial transcription factor Tfam. Our findings help us understand the mechanisms underlying the effects of exercise as a therapeutic intervention designed to trigger the pro-metabolic functions of p53.
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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.