ArticleCell metabolism2022
Mosaic dysfunction of mitophagy in mitochondrial muscle disease.
Article in Cell metabolism, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers, 1 of them a synthesis that pooled it.
What it found
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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.
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Who cites it
50 citing papers in PubMed, 1 synthesis or guideline pooled it, 85 citations in OpenAlex.
- Impact of scoliosis-specific exercises on adolescents with idiopathic scoliosis.BMC musculoskeletal disorders · 2025Pooled it
- Mitophagy coordinates organelle crosstalk in health and diseases.Signal transduction and targeted therapy · 2026Review
- Review
- Sustained loss ofbioRxiv : the preprint server for biology · 2026Article
- Mechanism of enteral nutrition in regulating Tfh/Tfr immune imbalance in colorectal cancer via the TLR4 signaling pathway.Journal of clinical biochemistry and nutrition · 2026Article
- The two faces of mitochondrial CaJournal of physiology and biochemistry · 2026Review
- Cis-3-hexen-1-ol suppresses bladder cancer progression by inducing mitophagy via the PCK2/AMPK/mTOR signaling pathway.Cellular oncology (Dordrecht, Netherlands) · 2026Article
- Beyond Membrane Remodeling: Organelle Crosstalk and Convergent Pathology in Centronuclear Myopathy.Muscles (Basel, Switzerland) · 2026Review
- Vitamin E alleviates energy stress-induced injury in yak granulosa cells by blocking the AMPK/mTOR-mitophagy-ferroptosis axis.Journal of ovarian research · 2026Article
- Review
- Targeting mitochondrial deubiquitinase USP30 to induce mitophagy in heteroplasmic mitochondrial diseases.Pharmacological reports : PR · 2026Article
- Activation of the protective arm of renin-angiotensin system enhances mitochondrial turnover improving respiration and decreasing integrated stress response in a human Complex III deficiency model.bioRxiv : the preprint server for biology · 2026Article
- Rescuing Mitochondrial Dysfunction in Macrophages Prevents Osteonecrosis of the Jaw in Anti-Resorptive Therapy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Lipopolysaccharide promotes bladder cancer immunosuppression by disrupting the Tfh/Tfr balance through TLR4 signaling.American journal of translational research · 2026Article
- Mitophagy in the pathogenesis and management of disease.Cell research · 2026Review
- Rab3A attenuated H₂O₂-induced mitochondrial dysfunction and damage in HEI-OC1 cells by stabilizing ITGA3 expression.Journal of bioenergetics and biomembranes · 2025Article
- A mitochondria-targeted fluoropolymer nanoparticle with inherent mitophagy-inducing and red fluorescence properties for treatment of atherosclerosis.Nature communications · 2025Article
- Perspectives on mitochondrial dysfunction in the regeneration of aging skeletal muscle.Cellular & molecular biology letters · 2025Review
- Harnessing tissue-derived mitochondria-rich extracellular vesicles (Ti-mitoEVs) to boost mitochondrial biogenesis for regenerative medicine.Science advances · 2025Article
- The mitophagy receptor BNIP3L/Nix coordinates nuclear calcium signaling to modulate the muscle phenotype.Autophagy · 2025Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
Mitophagy is a quality control mechanism that eliminates damaged mitochondria, yet its significance in mammalian pathophysiology and aging has remained unclear. Here, we report that mitophagy contributes to mitochondrial dysfunction in skeletal muscle of aged mice and human patients. The early disease stage is characterized by muscle fibers with central nuclei, with enhanced mitophagy around these nuclei. However, progressive mitochondrial dysfunction halts mitophagy and disrupts lysosomal homeostasis. Interestingly, activated or halted mitophagy occur in a mosaic manner even in adjacent muscle fibers, indicating cell-autonomous regulation. Rapamycin restores mitochondrial turnover, indicating mTOR-dependence of mitochondrial recycling in advanced disease stage. Our evidence suggests that (1) mitophagy is a hallmark of age-related mitochondrial pathology in mammalian muscle, (2) mosaic halting of mitophagy is a mechanism explaining mosaic respiratory chain deficiency and accumulation of pathogenic mtDNA variants in adult-onset mitochondrial diseases and normal aging, and (3) augmenting mitophagy is a promising therapeutic approach for muscle mitochondrial dysfunction.
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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.