.png){kind=icon}
.png){kind=icon}
Return
Microglia-mediated neuroinflammation in intracerebral hemorrhage: Pathological mechanisms and implications for therapeutic development (Review)
.png){kind=icon}
PRE
AI
F
C
L
O
B
D
X
G
G
DOI：10.3892/ijmm.2026.5766.png)
.png){kind=icon}
Original request for help.png){kind=icon}
Share.png){kind=icon}
Save
Abstract
En 中文
Intracerebral hemorrhage (ICH), a life-threatening subtype of stroke accounting for 10-15% of global stroke cases, is characterized by high disability and mortality rates, imposing a heavy socioeconomic burden worldwide. Despite its clinical importance, no effective therapeutic interventions exist for this condition. As the resident immune cells of the central nervous system, microglia play a pivotal role in the pathophysiology of ICH. These cells can be activated to adopt either anti-inflammatory or pro-inflammatory phenotypes. Following ICH, pro-inflammatory mediators derived from microglia act as key drivers of neuroinflammation, thereby exacerbating secondary brain injury. By contrast, promoting the phenotypic shift of microglia toward an anti-inflammatory state has been shown to mitigate an inflammatory response and facilitate neurological recovery. In the present study, existing evidence was reviewed to propose that post-ICH brain injury and repair are orchestrated not by isolated cells, but by a highly dynamic neuroimmune network centered on microglia. Elucidating the spatiotemporal dynamics and key communicative nodes within this network represents a critical frontier. Moving beyond the classical M1/M2 dichotomy to target this network contextually offers a promising and precise therapeutic aim for future investigations.
Keywords:
ICH
brain damage
microglial polarization
neuroprotection
inflammation
Journal
I
IF:
5.8
Papers:
5.7K
Citations:
1.7W
Organization
Cited Papers