Epigenetic regulation of the inflammatory response in stroke

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外文摘要：Stroke is classified as ischemic or hemorrhagic,and there are few effective treatments for either type.Immunologic mechanisms play a critical role in secondary brain injury following a stroke,which manifests as cytokine release,blood-brain barrier disruption,neuronal cell death,and ultimately behavioral impairment.Suppressing the inflammatory response has been shown to mitigate this cascade of events in experimental stroke models.However,in clinical trials of anti-inflammatory agents,long-term immunosuppression has not demonstrated significant clinical benefits for patients.This may be attributable to the dichotomous roles of inflammation in both tissue injury and repair,as well as the complex pathophysiologic inflammatory processes in stroke.Inhibiting acute harmful inflammatory responses or inducing a phenotypic shift from a pro-inflammatory to an anti-inflammatory state at specific time points after a stroke are alternative and promising therapeutic strategies.Identifying agents that can modulate inflammation requires a detailed understanding of the inflammatory processes of stroke.Furthermore,epigenetic reprogramming plays a crucial role in modulating post-stroke inflammation and can potentially be exploited for stroke management.In this review,we summarize current findings on the epigenetic regulation of the inflammatory response in stroke,focusing on key signaling pathways including nuclear factor-kappa B,Janus kinase/signal transducer and activator of transcription,and mitogen-activated protein kinase as well as inflammasome activation.We also discuss promising molecular targets for stroke treatment.The evidence to date indicates that therapeutic targeting of the epigenetic regulation of inflammation can shift the balance from inflammation-induced tissue injury to repair following stroke,leading to improved post-stroke outcomes.

外文关键词：

DNA methylationhistone modificationintracerebral hemorrhageischemic strokeneuroinflammationneuroprotectionnon-coding RNARNA methylationsubarachnoid hemorrhagetreatment

作者：

Jingyi Liang、Fei Yang、Zixiao Li、Qian Li

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作者单位：

School of Basic Medical Sciences,Capital Medical University,Beijing,China

Department of Neurobiology,School of Basic Medical Sciences,Capital Medical University,Beijing,China

Laboratory for Clinical Medicine,Beijing Key Laboratory of Neural Regeneration and Repair,Capital Medical University,Beijing,China

Department of Neurology,Beijing Tiantan Hospital,Capital Medical University,Beijing,China

China National Clinical Research Center for Neurological Diseases,Beijing Tiantan Hospital,Capital Medical University,Beijing,China

National Center for Healthcare Quality Management in Neurological Diseases,Beijing Tiantan Hospital,Capital Medical University,Beijing,China

Chinese Institute for Brain Research,Beijing,China

Research Unit of Artificial Intelligence in Cerebrovascular Disease,Chinese Academy of Medical Sci

Department of Biochemistry and Molecular Biology,School of Basic Medical Sciences,Capital Medical University,Beijing,China

Beijing Key Laboratory of Cancer Invasion and Metastasis Research,Capital Medical University,Beijing,China

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出版年：

2025

DOI：

10.4103/NRR.NRR-D-24-00672

中国神经再生研究(英文版)

中国康复医学会

中国神经再生研究(英文版)

影响因子：0.902

ISSN：1673-5374

年,卷(期)：2025.20(11)