纤维化
细胞外基质
信号转导
免疫系统
先天免疫系统
间质细胞
生物
疾病
癌症研究
炎症
医学
免疫学
病态的
干扰素
细胞生物学
细胞信号
自噬
细胞
基质金属蛋白酶
电池类型
细胞外
生物信息学
神经科学
作者
Lemeng Feng,Feng Zhang,Jiamin Cao,Wei Xiong
标识
DOI:10.1016/j.phrs.2025.107971
摘要
The cyclic GMP-AMP synthase (cGAS)-stimulator of interferon genes (STING) pathway serves as a central sensor of cytosolic DNA, orchestrating innate immune responses and maintaining tissue homeostasis. However, dysregulated activation of this signaling cascade has been implicated in chronic inflammation, aberrant tissue remodeling, and the development of fibrosis across multiple organs. Fibrosis, a pathological process characterized by excessive extracellular matrix deposition, underlies progressive dysfunction in the lungs, liver, kidneys, heart, and skin. Recent studies have revealed that abnormal cGAS-STING signaling influences both immune and stromal cell responses, thereby linking DNA sensing to fibrotic progression. In this review, we summarize the current understanding of cGAS-STING in fibrotic diseases, discuss its cellular and molecular mechanisms, and highlight therapeutic strategies targeting this pathway. These insights provide a comprehensive perspective on cGAS-STING as a potential intervention point for diverse fibrotic disorders.
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