ArticleCell2012
p53 opens the mitochondrial permeability transition pore to trigger necrosis.
Article in Cell, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 412 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
412 citing papers in PubMed, 1 synthesis or guideline pooled it, 725 citations in OpenAlex.
- The romantic history of signaling pathway discovery in cell death: an updated review.Molecular and cellular biochemistry · 2024Pooled it
- The Compatibility of Astragali Radix and Angelicae Sinensis Radix Attenuates Atherosclerosis by Suppressing Vascular Endothelial PANoptosis via the p38 MAPK/p53 Pathway: A Multi-Omics and Experimental Study.International journal of molecular sciences · 2026Article
- Advances in paclitaxel-mediated remodeling of the gastric cancer immune microenvironment and sensitization to immune checkpoint inhibitors via cGAS-STING pathway activation triggered by mtDNA release: challenges and translational perspectives.Molecular biology reports · 2026Review
- Mitochondrial Permeability Transition Regulators As Emerging Therapeutic Targets in Aging and Neurodegeneration: Recent Insights.Journal of molecular neuroscience : MN · 2026Review
- Mitochondrial quality control in health and disease: mechanisms and therapeutic targets.Signal transduction and targeted therapy · 2026Review
- Disruption of macrophage migration inhibitory factor signaling induces major tumor-associated macrophage phenotypes in human M2 macrophages.Molecular biomedicine · 2026Article
- Article
- Natural photosynthetic system for restoring homeostasis of animal organelle interaction network.Nature communications · 2026Article
- p53 Interacts with VDAC1, Modulating Its Expression Level and Oligomeric State to Activate Apoptosis.Biomolecules · 2026Article
- Ambiguous Role of p53 in Transcription-Dependent Tumor Cell Death.International journal of molecular sciences · 2026Review
- Article
- α-Lipoic acid suppresses p53 by preventing annexin A2 degradation to protect dopaminergic neurons in a Parkinson's disease model.Frontiers in neuroscience · 2026Article
- Tip60-HDAC8-SMURF2-mediated β-TrCP1 degradation is a key mechanism for hypoxia-induced cell death and tissue injury.Cellular and molecular life sciences : CMLS · 2025Article
- Si-Miao-Yong-An decoction suppresses necroptosis by regulating the p53 pathway in myocardial ischemia/reperfusion injury.Scientific reports · 2025Article
- VDAC1-interacting proteins: binding site mapping and their derived peptides induce apoptosis and multifaceted cellular effects.Apoptosis : an international journal on programmed cell death · 2025Article
- Mitochondrial transplantation attenuates alveolar epithelial cell dysfunction and reduces disruption of tight junction proteins to alleviate lung ischaemia-reperfusion injury.Journal of translational medicine · 2025Article
- Unlocking the potential of uncontrolled DCD in lung transplantation: A review of 2 decades of experience.JHLT open · 2025Review
- Depletion of oxysterol-binding proteins by OSW-1 triggers RIP1/RIP3-independent necroptosis and sensitization to cancer immunotherapy.Cell death and differentiation · 2025Article
- The absence of Parkin in hTau mice leads to synaptic mitochondrial dysfunction, alterations to the synaptic proteome, and increased phosphorylated tau in the Hippocampus.Neurobiology of disease · 2025Article
- Preclinical Models of Donation-After-Circulatory-Death and Brain-Death: Advances in Kidney Preservation and Transplantation.Biology · 2025Review
352 more citing papers are in PubMed but not listed here.
Corrections and comments
- Commented on by
- Commented on by
Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
Ischemia-associated oxidative damage leading to necrosis is a major cause of catastrophic tissue loss, and elucidating its signaling mechanism is therefore of paramount importance. p53 is a central stress sensor responding to multiple insults, including oxidative stress to orchestrate apoptotic and autophagic cell death. Whether p53 can also activate oxidative stress-induced necrosis is, however, unknown. Here, we uncover a role for p53 in activating necrosis. In response to oxidative stress, p53 accumulates in the mitochondrial matrix and triggers mitochondrial permeability transition pore (PTP) opening and necrosis by physical interaction with the PTP regulator cyclophilin D (CypD). Intriguingly, a robust p53-CypD complex forms during brain ischemia/reperfusion injury. In contrast, reduction of p53 levels or cyclosporine A pretreatment of mice prevents this complex and is associated with effective stroke protection. Our study identifies the mitochondrial p53-CypD axis as an important contributor to oxidative stress-induced necrosis and implicates this axis in stroke pathology.
Indexed as
Identifiers
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.