ReviewBiochimica et biophysica acta2011
Is mPTP the gatekeeper for necrosis, apoptosis, or both?
Review in Biochimica et biophysica acta, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 167 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
167 citing papers in PubMed, 1 synthesis or guideline pooled it, 330 citations in OpenAlex.
- Systematic review of Leber's hereditary optic neuropathy - Clinical diagnosis, genetics overview and current concepts of treatment.Indian journal of ophthalmology · 2026Pooled it
- Alpha-synuclein and mitochondrial permeability transition pore interactions in rotenone-induced Parkinson's disease models: neuroprotective promise of cyclosporine A.Biochemistry and biophysics reports · 2026Article
- Far-infrared irradiation restores mitochondrial dynamics to ameliorate ischemic stroke.Neural regeneration research · 2026Article
- Polyamine metabolism in ischemia reperfusion injury: common mitochondrial mechanisms and organ-specific differences.Journal of translational medicine · 2026Review
- Protective mechanisms of Sirtuin Family in myocardial ischemia-reperfusion injury and translational therapeutic perspectives.Molecular biology reports · 2026Review
- Kidney‑enriched lipid nanoparticles delivering ANXA2 alleviate renal ischemia-reperfusion injury via CHMP2A-mediated necroptosis inhibition.Journal of nanobiotechnology · 2026Article
- Regulation of Myogenic Cell Apoptosis, UPS, and Autophagy During Mammalian Skeletal Myogenesis.Cells · 2026Review
- Review
- Decoding the mechanisms of amyloid-β in synaptic toxicity.Journal of Alzheimer's disease : JAD · 2026Review
- CypD Dependent mPTP Opening Is Crucial for Oxidized Mitochondrial DNA Release in Ferroptosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Synergistic mitigation of endotoxin-induced liver injury by low-frequency PMF and 27.12 MHz RF-EMF: a multi-biomarker experimental study.European journal of trauma and emergency surgery : official publication of the European Trauma Society · 2026Article
- The role of mitochondria-endoplasmic reticulum crosstalk in colorectal cancer.Genes & diseases · 2026Review
- BAK and BAX: Therapeutic Targets for Acute Myocardial Infarction and Myocardial Ischemia-Reperfusion Injury.Biology · 2025Review
- UNI-494 treatment improves measures of renal dysfunction and cardiac pathology in male rats receiving L-NAME and angiotensin II.Physiological reports · 2025Article
- Reactive Oxygen Species Across Death Pathways: Gatekeepers of Apoptosis, Ferroptosis, Pyroptosis, Paraptosis, and Beyond.International journal of molecular sciences · 2025Review
- The Mitochondrial Permeability Transition Pore in Platelets: Mechanisms, Physiological Roles, and Therapeutic Perspectives.Antioxidants (Basel, Switzerland) · 2025Review
- Depletion of Mitochondrial Cyclophilin D in Endothelial and Smooth Muscle Cells Attenuates Vascular Dysfunction and Hypertension.Function (Oxford, England) · 2025Article
- Neuronal Injury after Ischemic Stroke: Mechanisms of Crosstalk Involving Necroptosis.Journal of molecular neuroscience : MN · 2025Review
- Calcium signaling in postsynaptic mitochondria: mechanisms, dynamics, and role in ATP production.Frontiers in molecular neuroscience · 2025Review
- MicroRNA-221 protects myocardial contractility in myocardial ischemia/reperfusion injury through phospholamban.PloS one · 2025Article
107 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Permeabilization of the mitochondrial membranes is a crucial step in apoptosis and necrosis. This phenomenon allows the release of mitochondrial death factors, which trigger or facilitate different signaling cascades ultimately causing the execution of the cell. The mitochondrial permeability transition pore (mPTP) has long been known as one of the main regulators of mitochondria during cell death. mPTP opening can lead to matrix swelling, subsequent rupture of the outer membrane, and a nonspecific release of intermembrane space proteins into the cytosol. While mPTP was purportedly associated with early apoptosis, recent observations suggest that mitochondrial permeabilization mediated by mPTP is generally more closely linked to events of late apoptosis and necrosis. Mechanisms of mitochondrial membrane permeabilization during cell death, involving three different mitochondrial channels, have been postulated. These include the mPTP in the inner membrane, and the mitochondrial apoptosis-induced channel (MAC) and voltage-dependent anion-selective channel (VDAC) in the outer membrane. New developments on mPTP structure and function, and the involvement of mPTP, MAC, and VDAC in permeabilization of mitochondrial membranes during cell death are explored. This article is part of a Special Issue entitled Mitochondria: the deadly organelle.
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What OpenQuestion holds
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.