内部收益率3
上睑下垂
坏死性下垂
刺
干扰素基因刺激剂
生物
干扰素
炎症体
钻机-I
细胞生物学
先天免疫系统
信号转导
线粒体DNA
自噬
程序性细胞死亡
免疫学
细胞凋亡
免疫系统
基因
遗传学
炎症
工程类
航空航天工程
作者
Lei Cai,Ying Tan,Dan Ni,Jin-Fu Peng,Guanghui Yi
标识
DOI:10.1016/j.cca.2022.04.003
摘要
Double stranded DNA (dsDNA) is known to act as a damage-associated molecular pattern (DAMP) that stimulates the body's innate immune response. In general, cyclicGMP-AMP(cGAMP)synthase(cGAS), a DNA sensor, detects these disease-causing DNA and activates the stimulator of interferon gene (STING), which in turn phosphorylates interferon regulatory factor 3 (IRF3), triggering the synthesis of type I interferon (IFN). During this process, the cGAS-STING pathway interacts with different modes of cell death, including autophagy, apoptosis, pyroptosis, and necroptosis. Importantly, cGAS might get stimulated by self-DNA, such as nuclear DNA (nuDNA) and mitochondrial DNA (mtDNA), which ensures a close association between the cGAS-STING signaling pathway and autoimmune responses. Following an ischemic attack, damaged or necrotic cells release large amounts of self-DNA that subsequently activate cGAS, resulting in a range of consequences related to an injury. The present study presents an overview of studies focused on cGAS-STING signaling and cell death, and summarizes the findings of this pathway with regard to ischemia or ischemia/reperfusion (I/R) in different organs of the body, including heart, brain, liver, kidney, and intestine.
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