ArticleCell cycle (Georgetown, Tex.)2013
Role of the c subunit of the FO ATP synthase in mitochondrial permeability transition.
Article in Cell cycle (Georgetown, Tex.), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 259 papers, 1 of them a synthesis that pooled it.
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Who cites it
259 citing papers in PubMed, 1 synthesis or guideline pooled it, 451 citations in OpenAlex.
- Comprehensive analysis of regulated cell death pathways: intrinsic disorder, protein-protein interactions, and cross-pathway communication.Apoptosis : an international journal on programmed cell death · 2025Pooled it
- Mitochondrial oxidative stress, calcium and dynamics in cardiac ischaemia-reperfusion injury.The Journal of physiology · 2026Review
- Mitochondrial homeostasis: the central hub governing the progression of atherosclerosis.Precision clinical medicine · 2026Review
- Mitochondrial permeability transition pore desensitization by a novel dispiranic derivative prevents cardiac reperfusion injury.Redox biology · 2026Article
- Reversing Mitochondrial Dysfunction in Optineurin E50K Glaucoma: A Metabolic Approach to Neuroprotection.Research square · 2026Article
- Fetal programming of the cardiac mitochondrial permeability transition pore in male offspring from hypoxic pregnancies.Redox biology · 2026Article
- Honokiol blocks tumor development and metastasis through mitochondrion-targeted effects.Cell death & disease · 2026Article
- Article
- Mitochondrial Protein Carboxyl-Terminal Alanine-Threonine Tailing Promotes Human Glioblastoma Growth by Regulating Mitochondrial Function.bioRxiv : the preprint server for biology · 2026Article
- Investigation of mitochondrial inner membrane ion conductance by planar lipid bilayer electrophysiology.Frontiers in physiology · 2026Article
- Yeast NatB Regulates Cell Death of Bax-Expressing Cells.Biomolecules · 2025Article
- Design and synthesis of 1,4,8-triazaspiro[4.5]decan-2-one derivatives as novel mitochondrial permeability transition pore inhibitors.Journal of enzyme inhibition and medicinal chemistry · 2025Article
- The innate immune receptor NLRX1 is a novel required modulator for mPTP opening: implications for cardioprotection.Basic research in cardiology · 2025Article
- Cryo-EM structure of the brine shrimp mitochondrial ATP synthase suggests an inactivation mechanism for the ATP synthase leak channel.Cell death and differentiation · 2025Article
- CYPD limits HRCell death discovery · 2025Article
- Differential Expression of Nuclear-Encoded Mitochondrial Protein Genes of ATP Synthase Across Different Tissues of Female Buffalo.Molecular biotechnology · 2025Article
- Modulation of mitochondrial permeability transition pores in reperfusion injury: Mechanisms and therapeutic approaches.European journal of clinical investigation · 2025Review
- Cyclophilin D (PPIF) and MPTP in hepatic ischemia-reperfusion injury: insights into mechanisms.Frontiers in immunology · 2025Review
- Sex Differences in Cardiac Tolerance to Oxygen Deprivation - 40 Years of Cardiovascular Research.Physiological research · 2024Review
- The Role of Mitochondrial Permeability Transition in Bone Metabolism, Bone Healing, and Bone Diseases.Biomolecules · 2024Review
199 more citing papers are in PubMed but not listed here.
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Authors and funding
14 authors at 5 institutions in 5 countries.
Funding
Abstract
The term "mitochondrial permeability transition" (MPT) refers to an abrupt increase in the permeability of the inner mitochondrial membrane to low molecular weight solutes. Due to osmotic forces, MPT is paralleled by a massive influx of water into the mitochondrial matrix, eventually leading to the structural collapse of the organelle. Thus, MPT can initiate mitochondrial outer membrane permeabilization (MOMP), promoting the activation of the apoptotic caspase cascade as well as of caspase-independent cell death mechanisms. MPT appears to be mediated by the opening of the so-called "permeability transition pore complex" (PTPC), a poorly characterized and versatile supramolecular entity assembled at the junctions between the inner and outer mitochondrial membranes. In spite of considerable experimental efforts, the precise molecular composition of the PTPC remains obscure and only one of its constituents, cyclophilin D (CYPD), has been ascribed with a crucial role in the regulation of cell death. Conversely, the results of genetic experiments indicate that other major components of the PTPC, such as voltage-dependent anion channel (VDAC) and adenine nucleotide translocase (ANT), are dispensable for MPT-driven MOMP. Here, we demonstrate that the c subunit of the FO ATP synthase is required for MPT, mitochondrial fragmentation and cell death as induced by cytosolic calcium overload and oxidative stress in both glycolytic and respiratory cell models. Our results strongly suggest that, similar to CYPD, the c subunit of the FO ATP synthase constitutes a critical component of the PTPC.
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