LAUSR

Macroautophagy (hereafter called autophagy), a highly programmed process maintains cellular homeostasis by degrading over-copious or damaged organelles, large macromolecular aggregates, and invading pathogens via the lysosomal system. Autophagy is generally activated by a variety of extracellular or intracellular stresses, such as oxygenor energy-deprivation, drugs, infections, etc. In addition to non-selective bulk degradation of cytosolic contents, autophagy selectively recycles specific organelles including mitochondria (mitophagy), endoplasmic reticulum (ER) (ER-phagy), lysosomes (lysosomophagy) and intracellular lipid droplets (lipophagy) (Eid. et al., 2013; Klionsky et al., 2021). Autophagy plays several important roles in the regulation of normal liver function and its dysregulation is associated with a wide variety of common and high-risk liver diseases such as metabolic associated fatty liver disease (MAFLD, previously called non-alcoholic fatty liver disease, NAFLD), alcoholic fatty liver disease (AFLD), hepatocellular carcinoma (HCC), and drug-induced liver injury (DILI) as well as their co-existing diseases such as obesity and type 2 diabetes mellitus (T2DM). Xenophagy, another type of selective autophagy which specifically targets intracellular pathogens include virophagy, a process being implicated in coronavirus disease 2019 (COVID-19)-associated hepatic pathologies (Liu et al., 2022). The focus of this Research Topic is to highlight the up-to-date mechanisms of selective and non-selective autophagy in liver and gut diseases. It complies one review article and three research articles. In a detailed review presented here, Alim Al-Bari et al. describe the mechanistic intricacies of selective autophagy and its impact on liver physiology and pathology and suggest modulation of selective autophagy as key to therapeutic interventions against several hepatic diseases. OPEN ACCESS