ArticleJournal of neuroinflammation2026
Targeting microglial C1q alleviates blood-brain barrier disruption in the thalamus after cortical infarction.
Article in Journal of neuroinflammation, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Focal cerebral infarction induces secondary damages in non-ischemic remote brain regions, severely affecting the prognosis and life quality of stroke patients. Disruption of blood–brain barrier (BBB) contributes to secondary thalamic damage after distal middle cerebral artery occlusion (dMCAO). However, the underlying molecular mechanisms that initiate BBB disruption and aggravate secondary thalamic damage after dMCAO remain unclear. It has been well-established that the complement pathway involves in the maintaining BBB integrity in the brain. Herein, using bulk RNA-sequencing and proteomics, we found that the complement pathway was the most pronounced in the ipsilateral ventroposterior nucleus (VPN) of thalamus at 2 weeks after dMCAO. Furthermore, we demonstrated for the first time that complement C1q derived mainly from a subtype of microglia binds to CD93 on endothelial cells, leading to the upregulation of vascular cell adhesion molecule 1 (VCAM-1) and BBB disruption in ipsilateral VPN after dMCAO. Knockdown of microglial C1q could inhibit the C1q-CD93 interaction, decrease VCAM-1 expression and maintain BBB integrity in the VPN, thus mitigating secondary thalamic damage after dMCAO. Moreover, minocycline treatment exerted neuroprotective effects by downregulating both microglial C1q and endothelial VCAM-1, consequently alleviating BBB disruption and neuronal loss in ipsilateral VPN, and improving neurological outcomes after dMCAO. Taken together, this innovative study highlights the pivotal role in maintaining BBB integrity mediated by microglial C1q in ipsilateral VPN after dMCAO. This finding provides a novel therapeutic target for improving the long-term prognosis of ischemic stroke patients.
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