ArticleCNS neuroscience & therapeutics2025
MK5 Regulates Microglial Activation and Neuroinflammation in Experimental Stroke Models.
Article in CNS neuroscience & therapeutics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Not yet cited in PubMed.
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Corrections and comments
- Erratum issued
Authors and funding
8 authors.
Funding
Abstract
objectiveMicroglial activation plays a crucial role in neuroinflammation following ischemic stroke. This study was conducted to investigate the role and potential mechanisms of MK5 within microglial cells in the inflammatory response following ischemic stroke in mice in vivo and in vitro.
methodsMicroglia-specific conditional MK5 knockout (MK5 cKO) mice and their control mice (MK5
resultsCompared to the control group, the knockout of the MK5 gene in microglia significantly exacerbated neurological deficits and increased infarct volume in MCAO mice. The loss of the MK5 promoted inflammation by upregulating pro-inflammatory factors and downregulating anti-inflammatory factors, while also enhancing microglial activation in both MCAO mice and BV2 microglial cells subjected to OGD/R. Furthermore, the knockout of the MK5 gene in microglia reduced the phosphorylation levels of HSP27 and increased the phosphorylation levels of NF-κB in the aforementioned models.
conclusionMicroglial MK5 plays a critical role in the ischemic neuroinflammatory response by regulating the phosphorylation of HSP27 and NF-κB, positioning it as a potential target for stroke treatment.
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