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Frontiers in Medical Science Research, 2025, 7(6); doi: 10.25236/FMSR.2025.070603.

Inflammation and Autophagy in Cerebral Hemorrhage: A Microglial Perspective

Author(s)

Xiaojie He1, Yi Zhang2

Corresponding Author:
Yi Zhang
Affiliation(s)

1Shaanxi University of Chinese Medicine, Xianyang, 712046, Shaanxi, China

2Affiliated Hospital of Shaanxi University of Chinese Medicine, Xianyang, 712000, Shaanxi, China

Abstract

Intracerebral hemorrhage (ICH) remains a devastating global health issue with high mortality and disability. Despite current supportive management strategies, there is a critical lack of treatments targeting the molecular pathways of neuronal death. The neurological injury post-ICH involves both primary damage from the hematoma and complex secondary injuries, where microglia play a central role. The polarization of activated microglia into pro-inflammatory M1 or anti-inflammatory/reparative M2 phenotypes is crucial; an imbalance towards sustained M1 activation exacerbates injury, while an M2 shift promotes repair. Emerging evidence highlights a critical crosstalk between inflammation and autophagy in regulating microglial function. Key signaling pathways, including the NLRP3 inflammasome and HMGB1/TLR4 axis, serve as molecular bridges in this dialogue. The outcome of this interaction significantly influences disease progression, where balanced autophagy can suppress excessive inflammation, but dysregulated autophagy can worsen damage. Therefore, elucidating and therapeutically targeting the key nodes within the microglial inflammation-autophagy crosstalk represents a highly promising avenue for developing novel neuroprotective strategies for ICH. 

Keywords

Intracerebral Hemorrhage; Autophagy; Secondary Brain Injury; Neuroinflammatory; Microglia; Mitophagy

Cite This Paper

Xiaojie He, Yi Zhang. Inflammation and Autophagy in Cerebral Hemorrhage: A Microglial Perspective. Frontiers in Medical Science Research (2025), Vol. 7, Issue 6: 22-31. https://doi.org/10.25236/FMSR.2025.070603.

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