TL;DR
It is suggested that C5aR1 serves as a regulatory factor in microglia-mediated neuroinflammation following ICH, and that targeting this pathway may offer a promising therapeutic strategy for hemorrhagic stroke.
Central post-stroke pain (CPSP) remains difficult to treat due to limited understanding of its underlying mechanisms. Emerging evidence implicates microglia-driven neuroinflammation in CPSP development. Mitogen-activated protein kinase phosphatase-1 (MKP-1) negatively regulates MAPK signaling and modulates inflammation...
BACKGROUND Secondary brain injury (SBI) following spontaneous intracerebral hemorrhage (ICH) is a critical determinant of neurological outcome. It is closely associated with neuronal death, and inflammatory responses. However, current research on SBI after ICH remains limited, and effective therapeutic targets are stil...
Chemokines are traditionally known for their roles in immune cell recruitment during inflammation, but emerging evidence suggests that they may also directly regulate cellular states within the central nervous system. Specifically, it remains unclear whether CXCL16 affects microglial functional states in ischemic strok...
Intracerebral hemorrhage (ICH) induces profound secondary brain injury, largely driven by dysregulated neuroinflammation, yet effective immunomodulatory therapies remain limited. Regulatory T (Treg) cells, a specialized subset of CD4+ T cells essential for immune tolerance and tissue repair, have emerged as critical mo...
Early brain injury (EBI) after subarachnoid hemorrhage (SAH) is closely associated with microglia-driven neuroinflammation, yet effective therapeutic strategies remain limited. Histone deacetylase 6 (HDAC6) has been implicated in neuroinflammatory regulation, but its role in microglial inflammatory activation after SAH...
Ischemic stroke induces complex neuroimmune responses that extend beyond acute neuronal injury and involve dynamic interactions among microglia, the neurovascular unit, and peripheral immune cells. Microglia rapidly transition from homeostatic surveillance to damage sensing, cytokine production, phagocytic clearance, a...
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