ArticleJournal of applied physiology (Bethesda, Md. : 1985)2022
Acute exercise rapidly activates hepatic mitophagic flux.
Article in Journal of applied physiology (Bethesda, Md. : 1985), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
21 citing papers in PubMed, 21 citations in OpenAlex.
- Exercise and dietary interventions in the regulation of hepatic mitophagy and liver recovery (Review).Biomedical reports · 2026Review
- Endurance exercise elicits temporal and sexual dimorphic multi-omics remodeling of liver metabolism revealed by MoTrPAC.Cell reports · 2026Article
- Hepatic ketogenic insufficiency blunts exercise-induced energy expenditure and alters mitochondrial proteins in skeletal muscle.Function (Oxford, England) · 2026Article
- Organellar insights in ageing and longevity.Nature cell biology · 2026Review
- Loss of ovarian function and estrogen therapy remodel the brain's synaptic and metabolic proteome.American journal of physiology. Regulatory, integrative and comparative physiology · 2026Article
- Accumulated mtDNA mutations are linked to specific impairments in NADH-linked respiration.iScience · 2026Article
- Physical exercise as a precision strategy for targeted PINK1 recruitment- a mechanistic review.Frontiers in physiology · 2026Review
- Loss of ovarian function and estrogen therapy remodel the brain's synaptic and metabolic proteome.bioRxiv : the preprint server for biology · 2025Article
- Hepatic ketogenic insufficiency blunts exercise-induced energy expenditure and alters mitochondrial proteins in skeletal muscle.bioRxiv : the preprint server for biology · 2025Article
- Loss of ovarian function prevents exercise-induced activation of hepatic mitophagic flux.American journal of physiology. Endocrinology and metabolism · 2025Article
- APOE4 Exerts Partial Diet-dependent Effects on Energy Expenditure and Skeletal Muscle Mitochondrial Pathways in a Preclinical Model.Function (Oxford, England) · 2025Article
- Exercise mitigates Alzheimer's disease by targeting ferroptosis driven by cellular senescence.Frontiers in cell and developmental biology · 2025Review
- Exercise regulates mitophagy to alleviate parkinsonian neurodegeneration.Frontiers in aging neuroscience · 2025Review
- The mitochondrial multi-omic response to exercise training across rat tissues.Cell metabolism · 2024Article
- Skeletal muscle proteome differs between youngFrontiers in aging neuroscience · 2024Article
- Review
- Sexually dimorphic hepatic mitochondrial adaptations to exercise: a mini-review.Journal of applied physiology (Bethesda, Md. : 1985) · 2023Review
- The mitochondrial multi-omic response to exercise training across tissues.bioRxiv : the preprint server for biology · 2023Article
- The Metabolic Basis for Nervous System Dysfunction in Alzheimer's Disease, Parkinson's Disease, and Huntington's Disease.Current neurovascular research · 2023Article
- The impact of aging and oxidative stress in metabolic and nervous system disorders: programmed cell death and molecular signal transduction crosstalk.Frontiers in immunology · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
Exercise is critical for improving metabolic health and putatively maintains or enhances mitochondrial quality control in metabolic tissues. Although previous work has shown that exercise elicits hepatic mitochondrial biogenesis, it is unknown if acute exercise activates hepatic mitophagy, the selective degradation of damaged or low-functioning mitochondria. We tested if an acute bout of treadmill running increased hepatic mitophagic flux both right after and 2-h postexercise in 15- to 24-wk-old C57BL/6J female mice. Acute exercise did not significantly increase markers of autophagic flux, however, mitophagic flux was activated 2-h post-treadmill running as measured by accumulation of both LC3-II and p62 in isolated mitochondria in the presence of leupeptin, an inhibitor of autophagosome degradation. Furthermore, mitochondrial-associated ubiquitin, which recruits the autophagy receptor protein p62, was also significantly increased at 2 h. Further examination via Western blot and proteomics analysis revealed that acute exercise elicits a time-dependent, dynamic activation of mitophagy pathways. Moreover, the results suggest that exercise-induced hepatic mitophagy is likely mediated by both polyubiquitination and receptor-mediated signaling pathways. Overall, we provide evidence that acute exercise activates hepatic mitophagic flux while also revealing specific receptor-mediated proteins by which exercise maintains mitochondrial quality control in the liver.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.