aGastrointestinal Unit, Center for the Study of Inflammatory Bowel Disease, Center for Computational and Integrative Biology, Massachusetts General Hospital, Boston, Massachusetts bBroad Institute of Harvard University and Massachusetts Institute of Technology, Cambridge, Massachusetts, USA.
Curr Opin Gastroenterol. 2013 Nov;29(6):588-96. doi: 10.1097/MOG.0b013e328365d34d.
From its initial description as a homeostatic process required for starvation response, autophagy has emerged as a ubiquitous cellular process involved in a broad range of cellular activities from metabolic adaptation to cellular defense against invading pathogens. This review provides an overview of autophagy and highlights the recent developments in deciphering its role in metabolic adaptation and its importance in antibacterial defense with attention to regulatory pathways.
Within the last 2 years, there has been significant progress in deciphering the mechanisms by which autophagy is regulated, including subcellular localization, posttranslational modifications, and transcriptional control. In addition, the cell type-specific role of autophagy in maintaining cellular homeostasis has been defined, including its role in handling intracellular pathogens and its contribution to inflammatory bowel disease.
Autophagy is a critical pathway that integrates numerous regulatory inputs to maintain cellular homeostasis and defend against intracellular pathogens.
自最初被描述为饥饿反应所需的一种稳态过程以来,自噬已成为一种普遍存在的细胞过程,涉及从代谢适应到细胞抵御入侵病原体的广泛细胞活动。本综述概述了自噬,并强调了最近在阐明其在代谢适应中的作用及其在抗菌防御中的重要性方面的进展,同时关注调控途径。
在过去的 2 年中,在阐明自噬调控的机制方面取得了重大进展,包括亚细胞定位、翻译后修饰和转录控制。此外,还定义了自噬在维持细胞内稳态中的细胞类型特异性作用,包括其在处理细胞内病原体和对炎症性肠病的贡献方面的作用。
自噬是一种关键途径,它整合了许多调控输入,以维持细胞内稳态并抵御细胞内病原体。