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Editorial: Autophagy and Related Transcription Factors in Liver and Gut Diseases

Year: 2020

Type: editorial

Abstract: The cell biologist Yoshinori Ohsumi received the 2016 Nobel Prize in Medicine for his early identification \nand characterization of the autophagy machinery, in particular, AuTophaGy-related (Atg) genes, in yeast. \nMacroautophagy (hereafter, autophagy) is a cytoprotective pathway for sequestration of cellular \ncomponents (such as misfolded proteins, damaged organelles, and excessive lipids) into \nautophagosomal vesicles, followed by clearance via the lysosomal system (Galluzzi et al., 2017). \nAutophagy is specifically upregulated upon exposure to various stressors such as oxidative and \nendoplasmic reticulum stress, thus aiding in the prevention of various pathologies. Therefore, \nautophagy dysregulation may be involved in inflammatory, metabolic, toxic, and infectious diseases \nand cancer (Kroemer et al., 2010; Eid et al., 2013; Horibe et al., 2017). Most organelles also seem to have \nselective programs of autophagy, including mitochondria, lipid droplets, endoplasmic reticulum, and even \nlysosomes. Selective autophagic removal of damaged mitochondria, or mitophagy, is an anti-apoptotic \nmechanism induced and specifically upregulated in response to various damaging agents such as binge \nethanol exposure or drug-induced liver injury in animal models (Otsuki et al., 1994; Youle and Narendra, \n2011; Lemasters, 2014; Eid et al., 2016; Eid et al., 2019). Autophagy can be regulated not only at the gene \nlevel, but its final performance can be modulated by lysosomal lipid composition.

Source: Frontiers in Pharmacology

DOI: 10.3389/fphar.2019.01610