上睑下垂
炎症体
程序性细胞死亡
半胱氨酸蛋白酶1
细胞生物学
糖尿病肾病
医学
癌症研究
炎症
细胞凋亡
免疫学
糖尿病
生物
内分泌学
生物化学
作者
Abdullah Al Mamun,Anjuman Ara Mimi,Yanqing Wu,Muhammad Zaeem,Md. Abdul Aziz,Suzia Aktar Suchi,Eman Alyafeai,Fahad Munir,Jian Xiao
标识
DOI:10.1016/j.cca.2021.09.003
摘要
Diabetic nephropathy (DN), a sterile inflammatory disease, is a serious complication of diabetes mellitus. However, recent evidence indicates that pyroptosis, a new term for pro-inflammatory cell death featured by gasdermin D (GSDMD)-stimulated plasma membrane pore generation, cell expansion and rapid lysis with the extensive secretion of pro-inflammatory factors, including interleukin-1β (IL-1β) and -18 (IL-18) may be involved in DN. Caspase-1-induced canonical and caspase-4/5/11-induced non-canonical inflammasome-signaling pathways are mainly believed to participate in pyroptosis-mediated cell death. Further research has uncovered that activation of the caspase-3/8 signaling pathway may also activate pyroptosis. Accumulating evidence has shown that NLRP3 inflammasome activation plays a critical role in promoting the pathogenesis of DN. In addition, current studies have suggested that pyroptosis-induced cell death promotes several diabetic complications that include DN. Our present study briefs the cellular mechanisms of pyroptosis-related signaling pathways and their impact on the promotion of DN. In this review, several investigational compounds suppressing pyroptosis-mediated cell death are explored as promising therapeutics in DN.
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