Mitogen-Activated Protein Kinase Signaling in Cerebral Ischemia
Summary
Mitogen-Activated Protein Kinase (MAPK) pathways constitute a pivotal intracellular signalling network that governs cellular fate in response to cerebral ischaemia. The MAPK family comprises three principal modules: extracellular signal-regulated kinases (ERK1/2), c-Jun N-terminal kinases (JNK) and p38 MAPKs. Under ischaemic conditions, excitotoxic glutamate release, oxidative stress and inflammatory mediators trigger upstream kinases, leading to phosphorylation cascades. Activated ERK1/2 may promote neuronal survival and plasticity, whereas JNK and p38 MAPK generally mediate apoptotic and pro-inflammatory programmes in the penumbral region. Temporal and spatial regulation of these kinases influences blood–brain barrier integrity, glial activation and neuronal apoptosis. Cross-talk between MAPK branches and other pathways, including NF-κB and apoptotic regulators, determines the balance between injury and recovery. Therapeutic inhibition or modulation of specific MAPK modules has shown promise in preclinical models, underscoring the global significance of targeting these kinases to limit infarct size, preserve neurological function and guide translational strategies for stroke.
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Mitogen-Activated Protein Kinase Signaling in Cerebral Ischemia publication trend
The graph below shows the total number of articles in mitogen-activated protein kinase signaling in cerebral ischemia across all publications each year (not limited to Nature Index journals).
Technical terms
Mitogen-Activated Protein Kinase (MAPK): A family of kinases transmitting extracellular stimuli into cellular responses via phosphorylation cascades.
ERK1/2: A MAPK subfamily primarily associated with cell survival, proliferation and synaptic plasticity.
JNK: Stress-activated MAPK subgroup that regulates apoptosis and inflammatory gene expression.
p38 MAPK: Stress-responsive kinase that mediates inflammatory cytokine production and cell death in ischaemic tissue.
Ischaemia–Reperfusion Injury: Tissue damage caused by the restoration of blood flow after an ischaemic episode, often exacerbating oxidative and inflammatory stress.
References
- p38 MAPK Endogenous Inhibition Improves Neurological Deficits in Global Cerebral Ischemia/Reperfusion Mice. Neural Plasticity (2022).
- Hyperglycemia aggravates ischemic brain damage via ERK1/2 activated cell autophagy and mitochondrial fission. Frontiers in Endocrinology (2022).
- GSK-126 Protects CA1 Neurons from H3K27me3-Mediated Apoptosis in Cerebral Ischemia. Molecular Neurobiology (2022).
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