ArticleAmerican journal of physiology. Renal physiology2010
Drp1 dephosphorylation in ATP depletion-induced mitochondrial injury and tubular cell apoptosis.
Article in American journal of physiology. Renal physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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Who cites it
47 citing papers in PubMed, 73 citations in OpenAlex.
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- Navigating the Complex Pathogenesis of Acute Kidney Injury: Exploring Macrophage Dynamics, Mitochondrial Dysfunction, and Ferroptosis Pathways.Advances in kidney disease and health · 2025Review
- Exploring the role and therapeutic potential of lipid metabolism in acute kidney injury.Renal failure · 2024Review
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- Magnesium Lithospermate B Protects Against Cisplatin-Induced Acute Kidney Injury via Alleviating Mitochondrial Dysfunction.Drug design, development and therapy · 2022Article
- Mitochondrial dysfunction in kidney injury, inflammation, and disease: Potential therapeutic approaches.Kidney research and clinical practice · 2020Review
- Extracellular vesicle-encapsulated IL-10 as novel nanotherapeutics against ischemic AKI.Science advances · 2020Article
- Protein Kinase C-Journal of the American Society of Nephrology : JASN · 2020Article
- Silibinin Induces G2/M Cell Cycle Arrest by Activating Drp1-Dependent Mitochondrial Fission in Cervical Cancer.Frontiers in pharmacology · 2020Article
- An Inhibitor of DRP1 (Mdivi-1) Alleviates LPS-Induced Septic AKI by Inhibiting NLRP3 Inflammasome Activation.BioMed research international · 2020Article
- Augmenter of Liver Regeneration Alleviates Renal Hypoxia-Reoxygenation Injury by Regulating Mitochondrial Dynamics in Renal Tubular Epithelial Cells.Molecules and cells · 2019Article
- Protective effect of cyclosporine A in the treatment of severe hydronephrosis in a rabbit renal pelvic perfusion modelTurkish journal of medical sciences · 2019Article
- Mitochondria in Sepsis-Induced AKI.Journal of the American Society of Nephrology : JASN · 2019Review
- MicroRNA-668 represses MTP18 to preserve mitochondrial dynamics in ischemic acute kidney injury.The Journal of clinical investigation · 2018Article
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- Dynamin-Related Protein 1 Deficiency Promotes Recovery from AKI.Journal of the American Society of Nephrology : JASN · 2018Article
- Mitochondrial energetics in the kidney.Nature reviews. Nephrology · 2017Review
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Recent studies revealed a striking morphological change of mitochondria during apoptosis. Mitochondria become fragmented and notably, the fragmentation contributes to mitochondrial outer membrane permeabilization and consequent release of apoptotic factors. In renal tubular cells, mitochondrial fragmentation involves the activation of Drp1, a key mitochondrial fission protein. However, it is unclear how Drp1 is regulated during tubular cell apoptosis. In this study, we examined Drp1 regulation during tubular cell apoptosis following ATP depletion. Rat kidney proximal tubular cells (RPTC) were subjected to azide treatment or severe hypoxia in glucose-free medium to induce ATP depletion. During ATP depletion, Drp1 was shown to be dephosphorylated at serine-637. Drp1 dephosphorylation could be suppressed by cyclosporine A and FK506, two calcineurin inhibitors. Importantly, cyclosporine A and FK506 could also prevent mitochondrial fragmentation, Bax accumulation, cytochrome c release, and apoptosis following ATP depletion in RPTC. The results suggest that calcineurin-mediated serine-637 dephosphorylation is involved in Drp1 activation during ATP depletion in renal tubular cells. Upon activation, Drp1 contributes to mitochondrial fragmentation and outer membrane permeabilization, resulting in the release of apoptogenic factors and apoptosis.
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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.