ReviewOncogene2015
Molecular mechanisms of cell death: central implication of ATP synthase in mitochondrial permeability transition.
Review in Oncogene, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 95 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
95 citing papers in PubMed, 1 synthesis or guideline pooled it, 337 citations in OpenAlex.
- The romantic history of signaling pathway discovery in cell death: an updated review.Molecular and cellular biochemistry · 2024Pooled it
- Dual-Action NSAID-Gold(I) Alkynyl Hybrids for Synergistic Anti-Inflammatory and Anticancer Therapy of Colorectal Cancer.Inorganic chemistry · 2026Article
- CypD Dependent mPTP Opening Is Crucial for Oxidized Mitochondrial DNA Release in Ferroptosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- The relationship between RSUME and VHL/HIF-1α signalling pathway in renal cell carcinoma.Archives of medical science : AMS · 2026Article
- BAK and BAX: Therapeutic Targets for Acute Myocardial Infarction and Myocardial Ischemia-Reperfusion Injury.Biology · 2025Review
- Sex differences in progressive multiple sclerosis brain gene expression in oligodendrocytes and OPCs.BMC medical genomics · 2025Article
- Identification and multi-dimensional validation of mitochondrial permeability transition-driven necrosis-related model to assess the prognosis and immunotherapy value in breast cancer.European journal of medical research · 2025Article
- Thermodynamic Considerations on the Biophysical Interaction between Low-Energy Electromagnetic Fields and Biosystems.Membranes · 2024Article
- Characterization of PDGF-Induced Subcellular Calcium Regulation through Calcium Channels in Airway Smooth Muscle Cells by FRET Biosensors.Biosensors · 2024Article
- HSK3486 Inhibits Colorectal Cancer Growth by Promoting Oxidative Stress and ATPase Inhibitory Factor 1 Activation.Digestive diseases and sciences · 2024Article
- Oligodendrocyte Maturation Alters the Cell Death Mechanisms That Cause Demyelination.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- Restoring the infected powerhouse: Mitochondrial quality control in sepsis.Redox biology · 2023Review
- The Interplay Between Autophagy and Regulated Necrosis.Antioxidants & redox signaling · 2023Review
- Fluid shear stress enhances proliferation of breast cancer cells via downregulation of the c-subunit of the FBiochemical and biophysical research communications · 2022Article
- Experimental and molecular docking studies of quercetin and vitamin E with diabetes-associated mitochondrial-ATPase as anti-apoptotic therapeutic strategies.Journal of diabetes and metabolic disorders · 2022Article
- Pharmacological and analytical aspects of alkannin/shikonin and their derivatives: An update from 2008 to 2022.Chinese herbal medicines · 2022Review
- Stabilization of SAMHD1 by NONO is crucial for Ara-C resistance in AML.Cell death & disease · 2022Article
- Assessing Drug-Induced Mitochondrial Toxicity in Cardiomyocytes: Implications for Preclinical Cardiac Safety Evaluation.Pharmaceutics · 2022Review
- Review
- Quercetin and vitamin E ameliorate cardio-apoptotic risks in diabetic rats.Molecular and cellular biochemistry · 2022Article
35 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issued
Authors and funding
7 authors at 5 institutions in 4 countries.
Funding
Abstract
The term mitochondrial permeability transition (MPT) is commonly used to indicate an abrupt increase in the permeability of the inner mitochondrial membrane to low molecular weight solutes. Widespread MPT has catastrophic consequences for the cell, de facto marking the boundary between cellular life and death. MPT results indeed in the structural and functional collapse of mitochondria, an event that commits cells to suicide via regulated necrosis or apoptosis. MPT has a central role in the etiology of both acute and chronic diseases characterized by the loss of post-mitotic cells. Moreover, cancer cells are often relatively insensitive to the induction of MPT, underlying their increased resistance to potentially lethal cues. Thus, intense efforts have been dedicated not only at the understanding of MPT in mechanistic terms, but also at the development of pharmacological MPT modulators. In this setting, multiple mitochondrial and extramitochondrial proteins have been suspected to critically regulate the MPT. So far, however, only peptidylprolyl isomerase F (best known as cyclophilin D) appears to constitute a key component of the so-called permeability transition pore complex (PTPC), the supramolecular entity that is believed to mediate MPT. Here, after reviewing the structural and functional features of the PTPC, we summarize recent findings suggesting that another of its core components is represented by the c subunit of mitochondrial ATP synthase.
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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.