ArticleThe Journal of cell biology2022
Mitochondrial dysfunction triggers actin polymerization necessary for rapid glycolytic activation.
Article in The Journal of cell biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 36 citations in OpenAlex.
- Disulfidptosis contributes to rotenone-induced dopaminergic neuron damage.Neural regeneration research · 2026Article
- InsP3R signaling and actomyosin-dependent mitochondrial dynamics play essential roles in mitochondrial stress-induced longevity.Nature communications · 2026Article
- Mechanisms of actin-binding proteins in glycolysis-cytoskeleton coupling.Journal of translational medicine · 2026Review
- Energy stress activates AMPK to arrest mitochondria via phosphorylation of TRAK1.The Journal of cell biology · 2026Article
- Autophagosome turnover requires Arp2/3 complex-mediated maintenance of lysosomal integrity.Molecular biology of the cell · 2026Article
- Pleiotropic regulation of mitochondrial translational factors in governing proliferation, apoptosis and metastasis during cancer progression.World journal of clinical oncology · 2026Review
- Metabolic costs and trade-offs of hypermetabolism in human motor neurons with ATP synthase deficiency.Communications biology · 2025Article
- Gastrodin inhibits hexokinase-2 mediated glycolysis to rescue rotenone-damaged PC12 cells.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- Heat-Induced Pathophysiological and Metabolic Changes at the Feto-Maternal Interface Predisposing to Preterm Birth.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Peri-mitochondrial actin filaments inhibit Parkin assembly by disrupting ER-mitochondria contacts.EMBO reports · 2025Article
- InsP3R signaling mediates mitochondrial stress-induced longevity through actomyosin-dependent mitochondrial dynamics.bioRxiv : the preprint server for biology · 2025Article
- Targeting pyruvate metabolism generates distinct CD8+ T cell responses to gammaherpesvirus and B lymphoma.JCI insight · 2025Article
- 3D printing cytoskeletal networks: ROS-induced filament severing leads to surge in actin polymerization.bioRxiv : the preprint server for biology · 2025Article
- Mitochondrial Dysfunction in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome.Physiology (Bethesda, Md.) · 2025Review
- Galectin-8 drives ERK-dependent mitochondrial fragmentation, perinuclear relocation and mitophagy, with metabolic adaptations for cell proliferation.European journal of cell biology · 2025Article
- Mitochondrial fission - changing perspectives for future progress.Journal of cell science · 2025Review
- Article
- Suppression of non-muscle myosin II boosts T cell cytotoxicity against tumors.Science advances · 2024Article
- Enhanced ROS Production and Mitochondrial Metabolic Shifts in CD4International journal of molecular sciences · 2024Article
- Axonal mitochondria regulate gentle touch response through control of axonal actin dynamics.bioRxiv : the preprint server for biology · 2024Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
Mitochondrial damage represents a dramatic change in cellular homeostasis. One rapid response is perimitochondrial actin polymerization, termed acute damage-induced actin (ADA). The consequences of ADA are not understood. In this study, we show evidence suggesting that ADA is linked to rapid glycolytic activation upon mitochondrial damage in multiple cells, including mouse embryonic fibroblasts and effector CD8+ T lymphocytes. ADA-inducing treatments include CCCP, antimycin, rotenone, oligomycin, and hypoxia. The Arp2/3 complex inhibitor CK666 or the mitochondrial sodium-calcium exchanger (NCLX) inhibitor CGP37157 inhibits both ADA and the glycolytic increase within 5 min, supporting ADA's role in glycolytic stimulation. Two situations causing chronic reductions in mitochondrial ATP production, mitochondrial DNA depletion and mutation to the NDUFS4 subunit of complex 1 of the electron transport chain, cause persistent perimitochondrial actin filaments similar to ADA. CK666 treatment causes rapid mitochondrial actin loss and a drop in ATP in NDUFS4 knock-out cells. We propose that ADA is necessary for rapid glycolytic activation upon mitochondrial impairment, to re-establish ATP production.
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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.