ReviewIUBMB life2021
Mitochondrial-nuclear p53 trafficking controls neuronal susceptibility in stroke.
Review in IUBMB life, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.
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.
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
26 citing papers in PubMed, 1 synthesis or guideline pooled it, 39 citations in OpenAlex.
- A systematic review and in silico analysis of studies investigating the ischemic penumbra proteome in animal models of experimental stroke.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2024Pooled it
- Decoding shared pathogenic networks of oxidative stress in neuropsychiatric disorders to prioritize multi-target therapeutics from natural products.Cell biology and toxicology · 2026Article
- Targeting DNA Damage and Repair Pathways in Cerebral Ischemic Stroke: From Bench to Bedside.Translational stroke research · 2026Review
- Comprehensive management of ischemic stroke with traditional Chinese medicine: a new exploration.Frontiers in medicine · 2026Review
- Exploring Therapeutic and Multitarget Mechanism of Molsidomine on Cerebral Ischemia: Molecular Docking and Multifaceted In Silico Study.Advances in experimental medicine and biology · 2026Article
- Effect ofPharmaceuticals (Basel, Switzerland) · 2025Article
- Role of autophagy in neurotoxic protein's clearance following post-ischemic stroke: where we are and what we know?Molecular brain · 2025Review
- The Role of Hydrogen Sulfide in the Localization and Structural-Functional Organization of p53 Following Traumatic Brain Injury: Development of a YOLO Model for Detection and Quantification of Apoptotic Nuclei.International journal of molecular sciences · 2025Article
- Modular-Based Synergetic Mechanisms of Jasminoidin and Ursodeoxycholic Acid in Cerebral Ischemia Therapy.Biomedicines · 2025Article
- Anticancer effects of purple carrot extract via induction of apoptotic genes on human breast cancer cells.Food science and biotechnology · 2025Article
- Differentially Expressed Genes in Rat Brain Regions with Different Degrees of Ischemic Damage.International journal of molecular sciences · 2025Article
- Sancai Lianmei granules ameliorate neuron injury in diabetic ischemic stroke rats by inhibiting oxidative stress and inflammation.Frontiers in endocrinology · 2025Article
- Chaperone-Mediated Autophagy Alleviates Cerebral Ischemia-Reperfusion Injury by Inhibiting P53-Mediated Mitochondria-Associated Apoptosis.Neurochemical research · 2024Article
- Suppression of neuronal CDK9/p53/VDAC signaling provides bioenergetic support and improves post-stroke neuropsychiatric outcomes.Cellular and molecular life sciences : CMLS · 2024Article
- The Relevance of Reperfusion Stroke Therapy for miR-9-3p and miR-9-5p Expression in Acute Stroke-A Preliminary Study.International journal of molecular sciences · 2024Article
- A New Benzo[6,7]oxepino[3,2-b] Pyridine Derivative Induces Apoptosis in Canine Mammary Cancer Cell Lines.Animals : an open access journal from MDPI · 2024Article
- The Interplay between Mitochondrial Dysfunction and Ferroptosis during Ischemia-Associated Central Nervous System Diseases.Brain sciences · 2023Review
- The ARTS of p53-dependent mitochondrial apoptosis.Journal of molecular cell biology · 2023Review
- mRNA and lncRNA co-expression network in mice of acute intracerebral hemorrhage.Frontiers in molecular neuroscience · 2023Article
- Novel insight into cGAS-STING pathway in ischemic stroke: from pre- to post-disease.Frontiers in immunology · 2023Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Stroke is a major cause of death and long-term disability in the adult. Neuronal apoptosis plays an essential role in the pathophysiology of ischemic brain damage and impaired functional recovery after stroke. The tumor suppressor protein p53 regulates key cellular processes, including cell cycle arrest, DNA repair, senescence, and apoptosis. Under cellular stress conditions, p53 undergoes post-translational modifications, which control protein localization, stability, and proapoptotic activity. After stroke, p53 rapidly accumulates in the ischemic brain, where it activates neuronal apoptosis through both transcriptional-dependent and -independent programs. Over the last years, subcellular localization of p53 has emerged as an important regulator of ischemia-induced neuronal apoptosis. Upon an ischemic insult, p53 rapidly translocates to the mitochondria and interacts with B-cell lymphoma-2 family proteins, which activate the mitochondrial apoptotic program, with higher efficacy than through its activity as a transcription factor. Moreover, the identification of a human single nucleotide polymorphism at codon 72 of the Tp53 gene that controls p53 mitochondrial localization and cell susceptibility to apoptosis supports the important role of the p53 mitochondrial program in neuronal survival and functional recovery after stroke. In this article, we review the relevance of mitochondrial and nuclear localization of p53 on neuronal susceptibility to cerebral ischemia and its impact on functional outcome of stroke patients.
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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.