Sadeghloo Zahra, Nabavi-Rad Ali, Zali Mohammad Reza, Klionsky Daniel J, Yadegar Abbas
Foodborne and Waterborne Diseases Research Center, Research Institute for Gastroenterology and Liver Diseases, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Gastroenterology and Liver Diseases Research Center, Research Institute for Gastroenterology and Liver Diseases, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Autophagy. 2025 Feb;21(2):260-282. doi: 10.1080/15548627.2024.2403277. Epub 2024 Oct 4.
Autophagy, a lysosome-dependent protein degradation mechanism, is a highly conserved catabolic process seen in all eukaryotes. This cell protection system, which is present in all tissues and functions at a basic level, can be up- or downregulated in response to various stresses. A disruption in the natural route of the autophagy process is frequently followed by an interruption in the inherent operation of the body's cells and organs. Probiotics are live bacteria that protect the host through various mechanisms. One of the processes through which probiotics exert their beneficial effects on various cells and tissues is autophagy. Autophagy can assist in maintaining host homeostasis by stimulating the immune system and affecting numerous physiological and pathological responses. In this review, we particularly focus on autophagy impairments occurring in several human illnesses and investigate how probiotics affect the autophagy process under various circumstances.: AD: Alzheimer disease; AKT: AKT serine/threonine kinase; AMPK: 5'AMP-activated protein kinase; ATG: autophagy related; CCl: carbon tetrachloride; CFS: cell-free supernatant; CMA: chaperone-mediated autophagy; CRC: colorectal cancer; EPS: H31 exopolysaccharide; HD: Huntington disease; HFD: high-fat diet; HPV: human papillomavirus; IFNG/IFN-γ: interferon gamma; IL6: interleukin 6; LGG: GG; LPS: lipopolysaccharide; MTOR: mechanistic target of rapamycin kinase; MTORC1: MTOR complex 1; NAFLD: non-alcoholic fatty liver disease; NASH: non-alcoholic steatohepatitis; PD: Parkinson disease; Pg3G: pelargonidin-3-O-glucoside; PI3K: phosphoinositide 3-kinase; PolyQ: polyglutamine; ROS: reactive oxygen species; SCFAs: short-chain fatty acids; SLAB51: a novel formulation of lactic acid bacteria and bifidobacteria; Slp: surface layer protein (of acidophilus NCFM); SNCA: synuclein alpha; ULK1: unc-51 like autophagy-activating kinase 1; YB: subsp. YB0411; YFP: yeast fermentate prebiotic.
自噬是一种依赖溶酶体的蛋白质降解机制，是在所有真核生物中都能见到的高度保守的分解代谢过程。这个存在于所有组织并在基础水平发挥作用的细胞保护系统，可根据各种应激而上调或下调。自噬过程的自然途径受到干扰后，人体细胞和器官的固有运作常常也会中断。益生菌是通过各种机制保护宿主的活细菌。益生菌对各种细胞和组织发挥有益作用的过程之一就是自噬。自噬可通过刺激免疫系统和影响众多生理及病理反应来帮助维持宿主体内平衡。在本综述中，我们特别关注几种人类疾病中出现的自噬损伤，并研究益生菌在各种情况下如何影响自噬过程。：AD：阿尔茨海默病；AKT：AKT丝氨酸/苏氨酸激酶；AMPK：5'AMP激活的蛋白激酶；ATG：自噬相关；CCl：四氯化碳；CFS：无细胞上清液；CMA：伴侣介导的自噬；CRC：结直肠癌；EPS：H31胞外多糖；HD：亨廷顿病；HFD：高脂饮食；HPV：人乳头瘤病毒；IFNG/IFN-γ：干扰素γ；IL6：白细胞介素6；LGG：GG；LPS：脂多糖；MTOR：雷帕霉素激酶的机制性靶点；MTORC1：MTOR复合物1；NAFLD：非酒精性脂肪性肝病；NASH：非酒精性脂肪性肝炎；PD：帕金森病；Pg3G：天竺葵素-3-O-葡萄糖苷；PI3K：磷脂酰肌醇3-激酶；PolyQ：聚谷氨酰胺；ROS：活性氧；SCFAs：短链脂肪酸；SLAB51：乳酸菌和双歧杆菌的新型制剂；Slp：（嗜酸乳杆菌NCFM的）表层蛋白；SNCA：α-突触核蛋白；ULK1：unc-51样自噬激活激酶1；YB：亚种YB0411；YFP：酵母发酵益生元
