Epigenetic regulation of the inflammatory response in stroke
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...
Saved in:
| Main Authors: | , , , |
|---|---|
| Format: | Article |
| Language: | English |
| Published: |
Wolters Kluwer Medknow Publications
2025-11-01
|
| Series: | Neural Regeneration Research |
| Subjects: | |
| Online Access: | https://journals.lww.com/10.4103/NRR.NRR-D-24-00672 |
| Tags: |
Add Tag
No Tags, Be the first to tag this record!
|
| _version_ | 1841556331523211264 |
|---|---|
| author | Jingyi Liang Fei Yang Zixiao Li Qian Li |
| author_facet | Jingyi Liang Fei Yang Zixiao Li Qian Li |
| author_sort | Jingyi Liang |
| collection | DOAJ |
| description | 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. |
| format | Article |
| id | doaj-art-178f5340dd394aeaa24acbe73c21a603 |
| institution | Kabale University |
| issn | 1673-5374 1876-7958 |
| language | English |
| publishDate | 2025-11-01 |
| publisher | Wolters Kluwer Medknow Publications |
| record_format | Article |
| series | Neural Regeneration Research |
| spelling | doaj-art-178f5340dd394aeaa24acbe73c21a6032025-01-07T09:49:28ZengWolters Kluwer Medknow PublicationsNeural Regeneration Research1673-53741876-79582025-11-0120113045306210.4103/NRR.NRR-D-24-00672Epigenetic regulation of the inflammatory response in strokeJingyi LiangFei YangZixiao LiQian LiStroke 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.https://journals.lww.com/10.4103/NRR.NRR-D-24-00672dna methylationhistone modificationintracerebral hemorrhageischemic strokeneuroinflammationneuroprotectionnon-coding rnarna methylationsubarachnoid hemorrhagetreatment |
| spellingShingle | Jingyi Liang Fei Yang Zixiao Li Qian Li Epigenetic regulation of the inflammatory response in stroke Neural Regeneration Research dna methylation histone modification intracerebral hemorrhage ischemic stroke neuroinflammation neuroprotection non-coding rna rna methylation subarachnoid hemorrhage treatment |
| title | Epigenetic regulation of the inflammatory response in stroke |
| title_full | Epigenetic regulation of the inflammatory response in stroke |
| title_fullStr | Epigenetic regulation of the inflammatory response in stroke |
| title_full_unstemmed | Epigenetic regulation of the inflammatory response in stroke |
| title_short | Epigenetic regulation of the inflammatory response in stroke |
| title_sort | epigenetic regulation of the inflammatory response in stroke |
| topic | dna methylation histone modification intracerebral hemorrhage ischemic stroke neuroinflammation neuroprotection non-coding rna rna methylation subarachnoid hemorrhage treatment |
| url | https://journals.lww.com/10.4103/NRR.NRR-D-24-00672 |
| work_keys_str_mv | AT jingyiliang epigeneticregulationoftheinflammatoryresponseinstroke AT feiyang epigeneticregulationoftheinflammatoryresponseinstroke AT zixiaoli epigeneticregulationoftheinflammatoryresponseinstroke AT qianli epigeneticregulationoftheinflammatoryresponseinstroke |