Neural Regeneration Research ›› 2025, Vol. 20 ›› Issue (11): 3045-3062.doi: 10.4103/NRR.NRR-D-24-00672

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Epigenetic regulation of the inflammatory response in stroke

Jingyi Liang1 , Fei Yang2, 3, Zixiao Li4, 5, 6, 7, 8, 9, *, Qian Li3, 10, 11, *   

  1. 1 School of Basic Medical Sciences, Capital Medical University, Beijing, China;  2 Department of Neurobiology, School of Basic Medical Sciences, Capital Medical University, Beijing, China;  3 Laboratory for Clinical Medicine, Beijing Key Laboratory of Neural Regeneration and Repair, Capital Medical University, Beijing, China;  4 Department of Neurology, Beijing Tiantan Hospital, Capital Medical University, Beijing, China;  5 China National Clinical Research Center for Neurological Diseases, Beijing Tiantan Hospital, Capital Medical University, Beijing, China;  6 National Center for Healthcare Quality Management in Neurological Diseases, Beijing Tiantan Hospital, Capital Medical University, Beijing, China;  7 Chinese Institute for Brain Research, Beijing, China;  8 Research Unit of Artificial Intelligence in Cerebrovascular Disease, Chinese Academy of Medical Sciences, Beijing, China;  9 Beijing Engineering Research Center of Digital Healthcare for Neurological Diseases, Beijing, China;  10Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Capital Medical University, Beijing, China;  11Beijing Key Laboratory of Cancer Invasion and Metastasis Research, Capital Medical University, Beijing, China
  • Online:2025-11-15 Published:2025-02-21
  • Contact: Zixiao Li, PhD, MD, lizixiao2008@hotmail.com; Qian Li, PhD, qianli@ccmu.edu.cn.
  • Supported by:
    This work was supported by the National Natural Science Foundation of China, Nos. 32070735 (to QL), 82371321 (to QL), 82171270 (to ZL); Public Service Platform for Artificial Intelligence Screening and Auxiliary Diagnosis for the Medical and Health Industry, Ministry of Industry and Information Technology of the People’s Republic of China, No. 2020-0103-3-1 (to ZL); the Natural Science Foundation of Beijing, No. Z200016 (to ZL); Beijing Talents Project, No. 2018000021223ZK03 (to ZL); and Beijing Municipal Committee of Science and Technology, No. Z201100005620010 (to ZL).

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Abstract: 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, longterm 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.

Key words: DNA methylation, histone modification, intracerebral hemorrhage, ischemic stroke, neuroinflammation, neuroprotection, non-coding RNA, RNA methylation, subarachnoid hemorrhage, treatment