ArticleCellular and molecular neurobiology2020
A Dual Role of ATM in Ischemic Preconditioning and Ischemic Injury.
Article in Cellular and molecular neurobiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 21 citations in OpenAlex.
- Circulating MicroRNA Profiling Identifies Distinct MicroRNA Signatures in Acute Ischemic Stroke and Transient Ischemic Attack Patients.International journal of molecular sciences · 2022Trial
- Targeting DNA Damage and Repair Pathways in Cerebral Ischemic Stroke: From Bench to Bedside.Translational stroke research · 2026Review
- Identification of Key Ferroptosis-Related Genes as Potential Diagnostic Biomarkers for Ischemic Stroke: Evidences from Integrated Bioinformatics Analysis and Experiments.Cellular and molecular neurobiology · 2025Article
- Transplantation of Neural Stem Cells-Overexpressed Ku70 Improves Neurological Deficits in a Mice Model of Cerebral Ischemia Stroke.Neurochemical research · 2024Article
- Monocyte, neutrophil, and whole blood transcriptome dynamics following ischemic stroke.BMC medicine · 2023Article
- GADD34 activates p53 and may have utility as a marker of atherosclerosis.Frontiers in medicine · 2023Article
- Identification of Genes Linking Natural Killer Cells to Apoptosis in Acute Myocardial Infarction and Ischemic Stroke.Frontiers in immunology · 2022Article
- Inhibition of PLK3 Attenuates Tubular Epithelial Cell Apoptosis after Renal Ischemia-Reperfusion Injury by Blocking the ATM/P53-Mediated DNA Damage Response.Oxidative medicine and cellular longevity · 2022Article
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
The ataxia-telangiectasia mutated (ATM) protein is regarded as the linchpin of cellular defenses to stress. Deletion of ATM results in strong oxidative stress and degenerative diseases in the nervous system. However, the role of ATM in neuronal ischemic preconditioning and lethal ischemic injury is still largely unknown. In this study, mice cortical neurons preconditioned with sublethal exposure to oxygen glucose deprivation (OGD) exhibited ATM/glucose-6-phosphate dehydrogenase pathway activation. Additionally, pharmacological inhibition of ATM prior to the preconditioning reversed neuroprotection provided by preconditioning in vitro and in vivo. Meanwhile, we found that ATM/P53 pro-apoptosis pathway was driven by lethal OGD injury, and pharmacological inhibition of ATM during fatal oxygen-glucose deprivation/reperfusion injury promoted neuronal survival. More importantly, inhibition of ATM activity after cerebral ischemia protected against cerebral ischemic-reperfusion damage in mice. In conclusion, our data show the dual role of ATM in neuronal ischemic preconditioning and lethal ischemic injury, involving in the protection of ischemic preconditioning, but promoting neuronal death in lethal ischemic injury. Thus, the present study provides new opportunity for the treatment of ischemic stroke.
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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.