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Microglial pyroptosis: Therapeutic target in secondary brain injury following intracerebral hemorrhage
Lingui Gu1, Mingjiang Sun1, Ruihao Li1
1Department of Neurosurgery, The Second Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Abstract:
Intracerebral hemorrhage (ICH) is a major cerebrovascular illness that causes substantial neurological sequelae and dysfunction caused by secondary brain injury (SBI), and there are no effective therapies to mitigate the disability. Microglia, the brain-resident macrophage, participates in the primary inflammatory response, and activation of microglia to an M1-like phenotype largely takes place in the acute phase following ICH. A growing body of research suggests that the pathophysiology of SBI after ICH is mediated by an inflammatory response mediated by microglial-pyroptotic inflammasomes, while inhibiting the activation of microglial pyroptosis could suppress the inflammatory cascade reaction, thus attenuating the brain injury after ICH. Pyroptosis is characterized by rapid plasma membrane disruption, followed by the release of cellular contents and pro-inflammatory mediators. In this review, we outline the molecular mechanism of microglial pyroptosis and summarize the up-to-date evidence of its involvement in the pathological process of ICH, and highlight microglial pyroptosis-targeted strategies that have the potential to cure intracerebral hemorrhage. This review contributes to a better understanding of the function of microglial pyroptosis in ICH and assesses it as a possible therapeutic target.
Insights
Intracerebral hemorrhage (ICH) causes significant brain injury. Targeting microglial pyroptosis, a cell death process, may offer a new therapy to reduce inflammation and brain damage after ICH.
Area of Science:
- Neuroscience
- Immunology
- Pathology
Background:
- Intracerebral hemorrhage (ICH) leads to severe neurological deficits due to secondary brain injury (SBI).
- Microglia, the brain's immune cells, become activated during the acute phase of ICH, contributing to inflammation.
- Current therapies for ICH are limited in mitigating long-term disability.
Purpose of the Study:
- To review the molecular mechanisms of microglial pyroptosis in ICH.
- To summarize evidence linking microglial pyroptosis to ICH pathology.
- To highlight potential therapeutic strategies targeting microglial pyroptosis for ICH.
Main Methods:
- Literature review focusing on microglial pyroptosis and its role in ICH.
- Analysis of molecular pathways involved in microglial activation and pyroptosis.
- Synthesis of current research on therapeutic interventions targeting microglial pyroptosis.
Main Results:
- Microglial pyroptosis, a pro-inflammatory form of cell death, is implicated in the secondary brain injury following ICH.
- Inhibition of microglial pyroptosis can suppress inflammatory responses and reduce brain damage.
- Pyroptosis involves rapid cell membrane rupture and release of inflammatory mediators.
Conclusions:
- Microglial pyroptosis plays a critical role in the pathophysiology of ICH.
- Targeting microglial pyroptosis presents a promising therapeutic avenue for treating intracerebral hemorrhage.
- Further research into microglial pyroptosis-targeted strategies could lead to effective treatments for ICH.
