ReviewMolecular neurobiology2021
Deregulated Protein Kinases: Friend and Foe in Ischemic Stroke.
Review in Molecular neurobiology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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.
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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
14 citing papers in PubMed, 26 citations in OpenAlex.
- Gata1-mediated Hras transcription stimulates blood-brain barrier injury in ischemic stroke through activation of the ERK pathway.Human cell · 2026Article
- Protein Kinase C Family: Structures, Biological Functions, Diseases, and Pharmaceutical Interventions.MedComm · 2025Review
- USP43 promotes cerebral ischemia-reperfusion injury via activation of TAK1.Cell & bioscience · 2025Article
- Mollugin attenuates oxygen-glucose deprivation/reperfusion-induced brain microvascular endothelial cell death and permeability through activation of BDNF/TrkB-modulated Akt pathway.Journal of bioenergetics and biomembranes · 2025Article
- Repurposing Cofilin-Targeting Compounds for Ischemic Stroke Through Cheminformatics and Network Pharmacology.Pharmaceuticals (Basel, Switzerland) · 2025Article
- Regulation of Blood-Brain Barrier Permeability via JNK Signaling Pathway: Mechanisms and Potential Therapeutic Strategies for Ischemic Stroke, Alzheimer's Disease and Brain Tumors.Molecules (Basel, Switzerland) · 2025Review
- Article
- Intestinal ischemia-reperfusion and blood-brain barrier compromise: pathways to cognitive dysfunction.Frontiers in neuroscience · 2025Review
- Assessment of blood-brain barrier injury in hypertensive CSVD by 11.7TMR T1mapping and microvascular pathologic changes.Metabolic brain disease · 2024Article
- Morphine Induced Neuroprotection in Ischemic Stroke by Activating Autophagy Via mTOR-Independent Activation of the JNK1/2 Pathway.Neurochemical research · 2024Article
- Network Analysis and Experimental Verification of the Mechanisms of Hydroxysafflor Yellow A in Ischemic Stroke Following Atherosclerosis.Molecules (Basel, Switzerland) · 2023Article
- Carbon dioxide and MAPK signalling: towards therapy for inflammation.Cell communication and signaling : CCS · 2023Review
- Emerging roles of astrocytes in blood-brain barrier disruption upon amyloid-beta insults in Alzheimer's disease.Neural regeneration research · 2023Review
- Post-stroke Impairment of the Blood-Brain Barrier and Perifocal Vasogenic Edema Is Alleviated by Endovascular Mesenchymal Stem Cell Administration: Modulation of the PKCδ/MMP9/AQP4-Mediated Pathway.Molecular neurobiology · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ischemic stroke is the third leading cause of mortality worldwide, but its medical management is still limited to the use of thrombolytics as a lifesaving option. Multiple molecular deregulations of the protein kinase family occur during the period of ischemia/reperfusion. However, experimental studies have shown that alterations in the expression of essential protein kinases and their pharmacological modulation can modify the neuropathological milieu and hasten neurophysiological recovery. This review highlights the role of key protein kinase members and their implications in the evolution of stroke pathophysiology. Activation of ROCK-, MAPK-, and GSK-3β-mediated pathways following neuronal ischemia/reperfusion injury in experimental conditions aggravate the neuropathology and delays recovery. Targeting ROCK, MAPK, and GSK-3β will potentially enhance myelin regeneration, improve blood-brain barrier (BBB) function, and suppress inflammation, which ameliorates neuronal survival. Conversely, protein kinases such as PKA, Akt, PKCα, PKCε, Trk, and PERK salvage neurons post-ischemia by mechanisms including enhanced toxin metabolism, restoring BBB integrity, neurotrophic effects, and apoptosis suppression. Certain protein kinases such as ERK1/2, JNK, and AMPK have favourable and unfavourable effects in salvaging ischemia-injured neurons. Targeting multiple protein kinase-mediated pathways simultaneously may improve neuronal recovery post-ischemia.
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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.