ReviewActa pharmacologica Sinica2011
CaMKII in cerebral ischemia.
Review in Acta pharmacologica Sinica, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers, 2 of them syntheses 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
75 citing papers in PubMed, 2 syntheses or guidelines pooled it, 146 citations in OpenAlex.
- A systematic review of alterations in sensorimotor networks following stroke: implications for integration and functional outcomes across recovery stages.Frontiers in neurology · 2025Pooled it
- Toxic Effects of Glyphosate on the Nervous System: A Systematic Review.International journal of molecular sciences · 2022Pooled it
- CaMKII as a Multimodal Signalling Hub in Neural Connectivity and Vulnerability.Molecular neurobiology · 2026Review
- Calcium/calmodulin-dependent protein kinase II inhibition using tatCN19o ameliorates spinal cord ischemia associated with aortic surgery.The Journal of thoracic and cardiovascular surgery · 2026Article
- The Janus face of CaMKII: from memory consolidation to neurotoxic switch in Alzheimer's disease.Archives of toxicology · 2025Review
- Role of CaMKIIa reticular neurons of caudal medulla in control of posture.Communications biology · 2025Article
- Radiofluorinated Analogs of NCS-382 as Potential PET Tracers for Imaging the CaMKIIα Hub Domain.ACS chemical neuroscience · 2025Article
- Role of CaMKII/CREB pathway in rapid-antidepressant-like effect: comparison of ketamine with rapastinel.Experimental brain research · 2025Article
- The neuroprotective γ-hydroxybutyrate analog 3-hydroxycyclopent-1-enecarboxylic acid does not directly affect CaMKIIα autophosphorylation at T286 or binding to GluN2B.Molecular pharmacology · 2025Article
- Oxygen/glucose-deprivation causes long-term impairment of synaptic CaMKII movement.bioRxiv : the preprint server for biology · 2025Article
- Brivaracitam Ameliorates Increased Inflammation, Oxidative Stress, and Acetylcholinesterase Activity in Ischemic Mice.Clinical psychopharmacology and neuroscience : the official scientific journal of the Korean College of Neuropsychopharmacology · 2025Article
- Zhongfeng Xingnao prescription alleviates injury of intracerebral hemorrhage via regulating the CaMKII/NF-κB p65/NLRP3/GSDMD signaling axis.Journal of traditional and complementary medicine · 2025Article
- Volatile oil ofFrontiers in pharmacology · 2025Review
- Selective inhibition of T-type calcium channel preserves ischemic pre-conditioning mediated neuroprotection during cerebral ischemia reperfusion injury in diabetic mice.Metabolic brain disease · 2024Article
- Ligand-induced CaMKIIα hub Trp403 flip, hub domain stacking, and modulation of kinase activity.Protein science : a publication of the Protein Society · 2024Article
- Mechanisms of Transsynaptic Degeneration in the Aging Brain.Aging and disease · 2024Review
- Unveiling the role of CaMKII in retinal degeneration: from biological mechanism to therapeutic strategies.Cell & bioscience · 2024Review
- [PI3K/Akt/Erk signaling pathway mediates neuroprotection of CaMKⅡγ and CaMKⅡδ against ischemic reperfusion injury in mice].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2024Article
- Calcium-Associated Proteins in Neuroregeneration.Biomolecules · 2024Review
- Novel insight into the therapeutical potential of flavonoids from traditional Chinese medicine against cerebral ischemia/reperfusion injury.Frontiers in pharmacology · 2024Review
15 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
Ischemic insults on neurons trigger excessive, pathological glutamate release that causes Ca²⁺ overload resulting in neuronal cell death (excitotoxicity). The Ca²⁺/calmodulin (CaM)-dependent protein kinase II (CaMKII) is a major mediator of physiological excitatory glutamate signals underlying neuronal plasticity and learning. Glutamate stimuli trigger autophosphorylation of CaMKII at T286, a process that makes the kinase "autonomous" (partially active independent from Ca²⁺ stimulation) and that is required for forms of synaptic plasticity. Recent studies suggested autonomous CaMKII activity also as potential drug target for post-insult neuroprotection, both after glutamate insults in neuronal cultures and after focal cerebral ischemia in vivo. However, CaMKII and other members of the CaM kinase family have been implicated in regulation of both neuronal death and survival. Here, we discuss past findings and possible mechanisms of CaM kinase functions in excitotoxicity and cerebral ischemia, with a focus on CaMKII and its regulation.
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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.