上睑下垂
炎症体
炎症
再灌注损伤
缺血
点头
炎症反应
半胱氨酸蛋白酶1
神经科学
医学
生物
免疫学
基因
生物化学
内科学
作者
Wanxing Duan,Xuejie Wang,Yaping Ma,Z Y Sheng,Huijuan Dong,Liying Zhang,Baogang Zhang,Maotao He
出处
期刊:Molecular Medicine Reports
[Spandidos Publications]
日期:2024-01-22
卷期号:29 (3)
标识
DOI:10.3892/mmr.2024.13170
摘要
Ischemic stroke poses a major threat to human health. Therefore, the molecular mechanisms of cerebral ischemia/reperfusion injury (CIRI) need to be further clarified, and the associated treatment approaches require exploration. The NOD‑like receptor thermal protein domain associated protein 3 (NLRP3) inflammasome serves an important role in causing CIRI, and its activation exacerbates the underlying injury. Activation of the NLRP3 inflammasome triggers the maturation and production of the inflammatory molecules IL‑1β and IL‑18, as well as gasdermin‑D‑mediated pyroptosis and CIRI damage. Thus, the NLRP3 inflammasome may be a viable target for the treatment of CIRI. In the present review, the mechanisms of the NLRP3 inflammasome in the intense inflammatory response and pyroptosis induced by CIRI are discussed, and the therapeutic strategies that target the NLRP3‑mediated inflammatory response and pyroptosis in CIRI are summarized. At present, certain drugs have already been studied, highlighting future therapeutic perspectives.
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