ArticleScience signaling2017
Mitochondrial redox signaling enables repair of injured skeletal muscle cells.
Article in Science signaling, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 papers.
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
79 citing papers in PubMed, 134 citations in OpenAlex.
- Exercise-related microRNAs in Caenorhabditis elegans regulate calcium homeostasis and mitochondrial dynamics: Conserved pathways, divergent microRNAs.The FEBS journal · 2026Article
- Intermittent AP-1 activation in muscles contributes to exercise-induced health benefits.bioRxiv : the preprint server for biology · 2026Article
- Effect of human adipose stem cell-derived mitochondrial transplantation on the activity of chronically injured anterior cruciate ligament cells.Bone & joint research · 2025Article
- Miro1 expression alters global gene expression, ERK1/2 phosphorylation, oxidation and cell cycle progression.Journal of cell science · 2025Article
- Recycle, repair, recover: the role of autophagy in modulating skeletal muscle repair and post-exercise recovery.Bioscience reports · 2025Review
- Biological resilience in health and disease.Disease models & mechanisms · 2024Review
- Mitochondrial mechanisms in the pathogenesis of chronic inflammatory musculoskeletal disorders.Cell & bioscience · 2024Review
- Mitochondrial heterogeneity and adaptations to cellular needs.Nature cell biology · 2024Review
- Patterning of the cell cortex by Rho GTPases.Nature reviews. Molecular cell biology · 2024Review
- An ex vivo animal model to study the effect of transverse mechanical loading on skeletal muscle.Communications biology · 2024Article
- Wound Repair of the Cell Membrane: Lessons fromCells · 2024Review
- Voluntary wheel running improves molecular and functional deficits in a murine model of facioscapulohumeral muscular dystrophy.iScience · 2024Article
- Mitochondria-encoded peptide MOTS-c participates in plasma membrane repair by facilitating the translocation of TRIM72 to membrane.Theranostics · 2024Article
- New insights into the role of cellular senescence and chronic wounds.Frontiers in endocrinology · 2024Review
- Early Endosomes Undergo Calcium-Triggered Exocytosis and Enable Repair of Diffuse and Focal Plasma Membrane Injury.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- Aging, oxidative stress and degenerative diseases: mechanisms, complications and emerging therapeutic strategies.Biogerontology · 2023Review
- Pitfalls of Mitochondrial Redox Signaling Research.Antioxidants (Basel, Switzerland) · 2023Review
- Energy (and Reactive Oxygen Species Generation) Saving Distribution of Mitochondria for the Activation of ATP Production in Skeletal Muscle.Antioxidants (Basel, Switzerland) · 2023Review
- Chronic Intermittent Hypoxia-Induced Diaphragm Muscle Weakness Is NADPH Oxidase-2 Dependent.Cells · 2023Article
- Peroxiredoxin 2 is required for the redox mediated adaptation to exercise.Redox biology · 2023Article
19 more citing papers are in PubMed but not listed here.
Corrections and comments
- Commented on byCa2017
Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Strain and physical trauma to mechanically active cells, such as skeletal muscle myofibers, injures their plasma membranes, and mitochondrial function is required for their repair. We found that mitochondrial function was also needed for plasma membrane repair in myoblasts as well as nonmuscle cells, which depended on mitochondrial uptake of calcium through the mitochondrial calcium uniporter (MCU). Calcium uptake transiently increased the mitochondrial production of reactive oxygen species (ROS), which locally activated the guanosine triphosphatase (GTPase) RhoA, triggering F-actin accumulation at the site of injury and facilitating membrane repair. Blocking mitochondrial calcium uptake or ROS production prevented injury-triggered RhoA activation, actin polymerization, and plasma membrane repair. This repair mechanism was shared between myoblasts, nonmuscle cells, and mature skeletal myofibers. Quenching mitochondrial ROS in myofibers during eccentric exercise ex vivo caused increased damage to myofibers, resulting in a greater loss of muscle force. These results suggest a physiological role for mitochondria in plasma membrane repair in injured cells, a role that highlights a beneficial effect of ROS.
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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.