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.
Findings suggest that MKP-1 may function as an endogenous negative regulator of microglia-mediated neuroinflammation following thalamic hemorrhage, and Pharmacological modulation of MKP-1 signaling warrants further investigation as a potential approach for CPSP.
CKLF1 is identified as a previously unrecognized regulator of neuronal ferroptosis following ICH through the CCR5/p38/p53 signaling pathway and is highlighted as a promising therapeutic target for precision treatment of hemorrhagic stroke.
This work demonstrated that recombinant CXCL16 (rCXCL16) modulated the expression of inflammation- and repair-associated markers in primary microglia and in the ischemic brain and suggested that its neuroprotective effects are associated with reduced inflammatory marker expression and attenuation of apoptotic injury af...
It is proposed that Treg-centered immunomodulation represents a promising but still underdeveloped therapeutic strategy for improving recovery after ICH and particular attention to emerging approaches such as antigen-specific CAR-Treg cells and gut–brain axis modulation.
Findings demonstrate that HDAC6 targeting attenuates SAH-induced EBI and improves neurological outcomes, at least partly by suppressing microglia-associated neuroinflammation and restoring inflammatory cytokine balance.
Therapeutic strategies should seek to redirect specific microglial programs rather than broadly suppress neuroinflammation, and potential approaches include modulating inflammasome and complement signaling, oxidative stress, phagocytosis, lipid metabolism, and repair-associated trophic functions.
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