ReviewOxidative medicine and cellular longevity2018
Cell Type-Specific Mechanisms in the Pathogenesis of Ischemic Stroke: The Role of Apoptosis Signal-Regulating Kinase 1.
Review in Oxidative medicine and cellular longevity, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 2 of them syntheses that pooled it.
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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.
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Who cites it
26 citing papers in PubMed, 2 syntheses or guidelines pooled it, 40 citations in OpenAlex.
- Cellular and Molecular Targets for Non-Invasive, Non-Pharmacological Therapeutic/Rehabilitative Interventions in Acute Ischemic Stroke.International journal of molecular sciences · 2022Pooled it
- Efficacy of adipose derived stem cells on functional and neurological improvement following ischemic stroke: a systematic review and meta-analysis.BMC neurology · 2020Pooled it
- Upregulation of Foxo3a protects neurons against hypoxia-ischaemia injury.Archives of medical science : AMS · 2026Article
- Article
- Flavonoids in Brain Ischemia-Reperfusion and their Effect on Kinases as Signaling Pathway Activity.CNS & neurological disorders drug targets · 2025Article
- Death-associated protein kinase 1: a double-edged sword in health and disease.Frontiers in immunology · 2025Review
- Comprehensive evaluation of Dragon's Blood in combination with borneol in ameliorating ischemic/reperfusion brain injury using RNA sequencing, metabolomics, and 16S rRNA sequencing.Frontiers in pharmacology · 2024Article
- Regulated necrosis pathways: a potential target for ischemic stroke.Burns & trauma · 2023Review
- Lysosomal-associated transmembrane protein 5 deficiency exacerbates cerebral ischemia/reperfusion injury.Frontiers in molecular neuroscience · 2022Article
- Serum and brain metabolomic study reveals the protective effects of Bai-Mi-Decoction on rats with ischemic stroke.Frontiers in pharmacology · 2022Article
- Dapsone, More than an Effective Neuro and Cytoprotective Drug.Current neuropharmacology · 2022Review
- Artemisinin attenuated ischemic stroke induced cell apoptosis through activation of ERK1/2/CREB/BCL-2 signaling pathwayInternational journal of biological sciences · 2022Article
- The Role of the ACE2/MasR Axis in Ischemic Stroke: New Insights for Therapy.Biomedicines · 2021Review
- Protective Effect of Naoxintong Capsule () Combined with Guhong Injection () on Rat Brain Microvascular Endothelial Cells during Cerebral Ischemia-Reperfusion Injury.Chinese journal of integrative medicine · 2021Article
- How cytosolic compartments play safeguard functions against neuroinflammation and cell death in cerebral ischemia.Metabolic brain disease · 2021Review
- CD4Oxidative medicine and cellular longevity · 2021Article
- Guhong Injection Alleviates Cerebral Ischemia-Reperfusion Injury via the PKC/HIF-1α Pathway in Rats.Frontiers in pharmacology · 2021Article
- Mir-184 Contributes to Brain Injury Through Targeting PPAP2B Following Ischemic Stroke in Male Rats.Frontiers in molecular neuroscience · 2021Article
- Disorder Genes Regulate the Progression of Ischemic Stroke through the NF-BioMed research international · 2021Article
- Protective Mechanism and Treatment of Neurogenesis in Cerebral Ischemia.Neurochemical research · 2020Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Stroke has become a more common disease worldwide. Despite great efforts to develop treatment, little is known about ischemic stroke. Cerebral ischemia activates multiple cascades of cell type-specific pathomechanisms. Ischemic brain injury consists of a complex series of cellular reactions in various cell types within the central nervous system (CNS) including platelets, endothelial cells, astrocytes, neutrophils, microglia/macrophages, and neurons. Diverse cellular changes after ischemic injury are likely to induce cell death and tissue damage in the brain. Since cells in the brain exhibit different functional roles at distinct time points after injury (acute/subacute/chronic phases), it is difficult to pinpoint genuine roles of cell types after brain injury. Many experimental studies have shown the association of apoptosis signal-regulating kinase 1 (ASK1) with cellular pathomechanisms after cerebral ischemia. Blockade of ASK1, by either pharmacological or genetic manipulation, leads to reduced ischemic brain injury and subsequent neuroprotective effects. In this review, we present the cell type-specific pathophysiology of the early phase of ischemic stroke, the role of ASK1 suggested by preclinical studies, and the potential use of ASK suppression, either by pharmacologic or genetic suppression, as a promising therapeutic option for ischemic stroke recovery.
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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.