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Autophagy is an evolutionarily conserved catabolic process that is essential for maintaining cellular, tissue, and organismal homeostasis. Autophagy-related (ATG) genes are indispensable for autophagosome formation. ATG3 is one of the key genes involved in autophagy, and its homologs are common in eukaryotes. During autophagy, ATG3 acts as an E2 ubiquitin-like conjugating enzyme in the ATG8 conjugation system, contributing to phagophore elongation. ATG3 has also been found to participate in many physiological and pathological processes in an autophagy-dependent manner, such as tumor occurrence and progression, ischemia–reperfusion injury, clearance of pathogens, and maintenance of organelle homeostasis. Intriguingly, a few studies have recently discovered the autophagy-independent functions of ATG3, including cell differentiation and mitosis. Here, we summarize the current knowledge of ATG3 in autophagosome formation, highlight its binding partners and binding sites, review its autophagy-dependent functions, and provide a brief introduction into its autophagy-independent functions.

Non-alcoholic fatty liver disease (NAFLD) is the fastest-growing liver disease in the world. Despite targeted agents which are needed to provide permanent benefits for patients with NAFLD, no drugs have been approved to treat NASH. Thyroid hormone is an important signaling molecule to maintain normal metabolism, and in vivo and vitro studies have shown that regulation of the 3,5,3’-triiodothyronine (T3)/ thyroid hormone receptor (TR) axis is beneficial not only for metabolic symptoms but also for the improvement of NAFLD and even for the repair of liver injury. However, the non-selective regulation of T3 to TR subtypes (TRα/TRβ) could cause unacceptable side effects represented by cardiotoxicity. To avoid deleterious effects, TRβ-selective thyromimetics were developed for NASH studies in recent decades. Herein, we will review the development of thyroid hormones and synthetic thyromimetics based on TR selectivity for NAFLD, and analyze the role of TR-targeted drugs for the treatment of NAFLD in the future.

One-dimensional polyaniline@halloysite (PANI@HA) nanotubes with enhanced selective oxidation activity of cyclohexene are fabricated by employing aniline (ANI) chemical polymerization on halloysite nanotubes in situ. By facilely controlling the doping acid, acidity, and ANI/HA weight ratio during the fabrication, PANI with a controllable doping degree, redox state, and content is grown on halloysite nanotubes. The cyclohexene selective oxidation result shows that PANI@HA nanotubes are effective catalysts in a solvent-free reaction system with H2O2 as the oxidant, and their catalytic activity relies on the doping acid, acidity, and ANI/HA weight ratio in the fabrication. PANI@HA synthesized with HCl as a doping acid to condition the acidity at 1 M and 2.04 ANI/HA weight ratio (PANI@HA/1 M/2.04-HCl) demonstrates highest catalytic activity (98.17% conversion and 99.50% selectivity to 1,2-cyclohexanediol). The cyclohexene selective catalytic activity matches well with the PANI doping degree in PANI@HA. In addition, the optimal reaction condition is 20 mg catalyst, 2.5 mL H2O2, 70 °C, and 24 h. Furthermore, PANI@HA/1 M/2.04-HCl exhibits superior dihydroxylation activity toward 2,3-dimethyl-2-butene and cycling performance with 99.11% conversion and 96.92% selectivity to 1,2-cyclohexanediol after five cycles. The CV of PANI@HA indicates that the cyclohexene selective oxidation is attributed to a reversible redox reaction of PANI in PANI@HA for catalytic decomposition of H2O2.