ArticleThe Biochemical journal2004
Cyclophilin-D promotes the mitochondrial permeability transition but has opposite effects on apoptosis and necrosis.
Article in The Biochemical journal, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers, 1 of them a synthesis that pooled it.
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Who cites it
56 citing papers in PubMed, 1 synthesis or guideline pooled it, 159 citations in OpenAlex.
- Topical cyclosporine A therapy for dry eye syndrome.The Cochrane database of systematic reviews · 2019Pooled it
- Fetal programming of the cardiac mitochondrial permeability transition pore in male offspring from hypoxic pregnancies.Redox biology · 2026Article
- Time-Resolved Metabolomics Reveals Mitochondrial Protection in Septic Liver Injury.Metabolites · 2025Article
- New advances in medical management of dry eye: optimizing treatment strategies for enhanced relief.International ophthalmology · 2024Review
- Surveying the landscape of emerging and understudied cell death mechanisms.Biochimica et biophysica acta. Molecular cell research · 2023Review
- Calcium Ions Signaling: Targets for Attack and Utilization by Viruses.Frontiers in microbiology · 2022Review
- Regulated cell death in cisplatin-induced AKI: relevance ofAmerican journal of physiology. Renal physiology · 2021Article
- Chrysophanol localizes in mitochondria to promote cell death through upregulation of mitochondrial cyclophilin D in HepG2 cells.Chinese herbal medicines · 2021Article
- Mitochondrial Permeability Transition: A Pore Intertwines Brain Aging and Alzheimer's Disease.Cells · 2021Review
- Physiopathology of the Permeability Transition Pore: Molecular Mechanisms in Human Pathology.Biomolecules · 2020Review
- Down-regulation of miRNA-27b-3p suppresses keratinocytes apoptosis in oral lichen planus.Journal of cellular and molecular medicine · 2019Article
- Practical guidance for the use of cyclosporine ophthalmic solutions in the management of dry eye disease.Clinical ophthalmology (Auckland, N.Z.) · 2019Article
- Inhibition of HOX/PBX dimer formation leads to necroptosis in acute myeloid leukemia cells.Oncotarget · 2017Article
- Cyclophilin D ablation is associated with increased end-ischemic mitochondrial hexokinase activity.Scientific reports · 2017Article
- Mitochondrial permeability transition in cardiac ischemia-reperfusion: whether cyclophilin D is a viable target for cardioprotection?Cellular and molecular life sciences : CMLS · 2017Review
- Characterization of cyclophilin D in freshwater pearl mussel (Zoological research · 2017Article
- Functionally and morphologically damaged mitochondria observed in auditory cells under senescence-inducing stress.NPJ aging and mechanisms of disease · 2017Article
- Impaired mitochondrial homeostasis and neurodegeneration: towards new therapeutic targets?Journal of bioenergetics and biomembranes · 2015Review
- Molecular regulation of auditory hair cell death and approaches to protect sensory receptor cells and/or stimulate repair following acoustic trauma.Frontiers in cellular neuroscience · 2015Review
- Essential versus accessory aspects of cell death: recommendations of the NCCD 2015.Cell death and differentiation · 2015Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Cyclophilin-D is a peptidylprolyl cis-trans isomerase of the mitochondrial matrix. It is involved in mitochondrial permeability transition, in which the adenine nucleotide translocase of the inner membrane is transformed from an antiporter to a non-selective pore. The permeability transition has been widely considered as a mechanism in both apoptosis and necrosis. The present study examines the effects of cyclophilin-D on the permeability transition and lethal cell injury, using a neuronal (B50) cell line stably overexpressing cyclophilin-D in mitochondria. Cyclophilin-D overexpression rendered isolated mitochondria far more susceptible to the permeability transition induced by Ca2+ and oxidative stress. Similarly, cyclophilin-D overexpression brought forward the onset of the permeability transition in intact cells subjected to oxidative stress. In addition, in the absence of stress, the mitochondria of cells overexpressing cyclophilin-D maintained a lower inner-membrane potential than those of normal cells. All these effects of cyclophilin-D overexpression were abolished by cyclosporin A. It is concluded that cyclophilin-D promotes the permeability transition in B50 cells. However, cyclophilin-D overexpression had opposite effects on apoptosis and necrosis; whereas NO-induced necrosis was promoted, NO- and staurosporine-induced apoptosis were inhibited. These findings indicate that the permeability transition leads to cell necrosis, but argue against its involvement in apoptosis.
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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.