自噬
胰岛素抵抗
串扰
代谢综合征
肠道菌群
平衡
ATG16L1
生物
炎症
失调
胰岛素
细胞生物学
生物信息学
内分泌学
糖尿病
免疫学
生物化学
细胞凋亡
物理
光学
作者
Jinyue Zhao,Liyun Duan,Jiarui Li,Chensi Yao,Guoqiang Wang,Jia Mi,Yong‐Jiang Yu,Liuqian Ding,Yunyun Zhao,Guanchi Yan,Jing Li,Zhixuan Zhao,Xiuge Wang,Min Li
标识
DOI:10.1016/j.biopha.2024.116807
摘要
Metabolic syndrome (MetS) is a widespread and multifactorial disorder, and the study of its pathogenesis and treatment remains challenging. Autophagy, an intracellular degradation system that maintains cellular renewal and homeostasis, is essential for maintaining antimicrobial defense, preserving epithelial barrier integrity, promoting mucosal immune response, maintaining intestinal homeostasis, and regulating gut microbiota and microbial metabolites. Dysfunctional autophagy is implicated in the pathological mechanisms of MetS, involving insulin resistance (IR), chronic inflammation, oxidative stress, and endoplasmic reticulum (ER) stress, with IR being a predominant feature. The study of autophagy represents a valuable field of research with significant clinical implications for identifying autophagy-related signals, pathways, mechanisms, and treatment options for MetS. Given the multifactorial etiology and various potential risk factors, it is imperative to explore the interplay between autophagy and gut microbiota in MetS more thoroughly. This will facilitate the elucidation of new mechanisms underlying the crosstalk among autophagy, gut microbiota, and MetS, thereby providing new insights into the diagnosis and treatment of MetS.
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