Thrap3 promotes nonalcoholic fatty liver disease by suppressing AMPK-mediated autophagy

Experimental & Molecular Medicine, Published online: 01 August 2023; doi:10.1038/s12276-023-01047-4A protein that interferes with a critical cellular housekeeping mechanism offers a promising drug target for non-alcoholic fatty liver disease (NAFLD), a condition that can lead to liver failure. Jang Hyun Choi of the Ulsan National Institute of Science and Technology, South Korea, and colleagues previously demonstrated that a protein called Thrap3 contributes to obesity-related insulin resistance. They have now investigated Thrap3 function in the liver and found that levels were significantly elevated in tissues from NAFLD patients. The researchers demonstrated that they could reduce NAFLD-associated lipid accumulation by using genetic techniques to shut down Thrap3 expression in liver cells. Thrap3 was found to inhibit autophagy, a cellular process for clearing out defective proteins and organelles. Impaired autophagy is a known contributor to NAFLD, and the authors hypothesize that Thrap3 inhibition could protect against this impairment.
Source: Experimental and Molecular Medicine - Category: Molecular Biology Authors: Source Type: research