ReviewBiochimica et biophysica acta2015
Structural mechanisms of cyclophilin D-dependent control of the mitochondrial permeability transition pore.
Review in Biochimica et biophysica acta, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
58 citing papers in PubMed, 107 citations in OpenAlex.
- Blocking mitochondrial cyclophilin D ameliorates TSH-impaired defensive barrier of artery.Redox biology · 2018Trial
- Role of voltage-dependent anion channel 1 in neurodegeneration: Mechanisms, implications, and therapeutic potential.Neural regeneration research · 2026Article
- Low-intensity transcranial ultrasound neuromodulation promotes neuronal regeneration: A new hope for noninvasive treatment of neurodegenerative diseases.Neural regeneration research · 2026Article
- The Mitochondrial Permeability Transition Pore in Platelets: Mechanisms, Physiological Roles, and Therapeutic Perspectives.Antioxidants (Basel, Switzerland) · 2025Review
- Mitochondrial DNA signals driving immune responses: Why, How, Where?Cell communication and signaling : CCS · 2025Review
- Cerium-based nanoplatform for severe acute pancreatitis: Achieving enhanced anti-inflammatory effects through calcium homeostasis restoration and oxidative stress mitigation.Materials today. Bio · 2025Article
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- Endogenous complement 1q binding protein (C1qbp) regulates mitochondrial permeability transition and post-myocardial infarction remodeling and dysfunction.Journal of molecular and cellular cardiology · 2024Article
- Mitochondrial CypD Acetylation Promotes Endothelial Dysfunction and Hypertension.Circulation research · 2024Article
- New cyclophilin D inhibitor rescues mitochondrial and cognitive function in Alzheimer's disease.Brain : a journal of neurology · 2024Article
- Tissue-specific differences in CaPhysiological reports · 2024Article
- Article
- Mechanism and treatment of intracerebral hemorrhage focus on mitochondrial permeability transition pore.Frontiers in molecular neuroscience · 2024Review
- Review
- Article
- Diplacone Isolated fromInternational journal of molecular sciences · 2023Article
- Current and future therapeutic strategies for Alzheimer's disease: an overview of drug development bottlenecks.Frontiers in aging neuroscience · 2023Review
- Energy metabolism disturbance in migraine: From a mitochondrial point of view.Frontiers in physiology · 2023Review
- Review
- Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
backgroundOpening of the mitochondrial permeability transition pore is the underlying cause of cellular dysfunction during diverse pathological situations. Although this bioenergetic entity has been studied extensively, its molecular componentry is constantly debated. Cyclophilin D is the only universally accepted modulator of this channel and its selective ligands have been proposed as therapeutic agents with the potential to regulate pore opening during disease. SCOPE OF REVIEW: This review aims to recapitulate known molecular determinants necessary for Cyclophilin D activity regulation and binding to proposed pore constituents thereby regulating the mitochondrial permeability transition pore. MAJOR
conclusionsWhile the main target of Cyclophilin D is still a matter of further research, permeability transition is finely regulated by post-translational modifications of this isomerase and its catalytic activity facilitates pore opening. GENERAL SIGNIFICANCE: Complete elucidation of the molecular determinants required for Cyclophilin D-mediated control of the mitochondrial permeability transition pore will allow the rational design of therapies aiming to control disease phenotypes associated with the occurrence of this unselective channel. This article is part of a Special Issue entitled Proline-directed Foldases: Cell Signaling Catalysts and Drug Targets.
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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.