Epigenetic regulation of the inflammatory response in stroke
Jingyi Liang1
Fei Yang2
Zixiao Li3
Qian Li4
1.School of Basic Medical Sciences,Capital Medical University,Beijing,China2.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,China3.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 Sciences,Beijing,China;Beijing Engineering Research Center of Digital Healthcare for Neurological Diseases,Beijing,China4.Laboratory for Clinical Medicine,Beijing Key Laboratory of Neural Regeneration and Repair,Capital Medical University,Beijing,China;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
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.
机标关键词：strokeepigeneticinflammatoryregulationresponse
论文发表日期：2025-11-27
在线出版日期：2025-08-15（本平台首次上网日期，不代表文献的发表时间）
页数：18( 3045-3062 )
英文信息