粒体自噬
上睑下垂
炎症
细胞生物学
自噬
炎症体
化学
半胱氨酸蛋白酶1
程序性细胞死亡
生物
细胞凋亡
免疫学
生物化学
受体
作者
Ranran Zhang,Shuang Guan,Zhuoqun Meng,Xuming Deng,Jing Lu
标识
DOI:10.1021/acs.jafc.4c01994
摘要
-chlorophenylhydrazone (CCCP) and rapamycin (Rapa). Thus, our results showed that 3-MCPD could induce mitochondrial damage and produce ROS. 3-MCPD suppressed mitophagy, leading to the accumulation of damaged mitochondria and ROS, thereby activating NLRP3 and pyroptosis. Meanwhile, 3-MCPD-mediated suppression of ESCRT-III hindered the repair of GSDMD-induced cell membrane rupture, which further caused the occurrence of pyroptosis. Our findings provide new perspectives for studying the mechanisms underlying 3-MCPD-induced renal injury.
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