USP13 ameliorates nonalcoholic fatty liver disease through inhibiting the activation of TAK1.

ABSTRACT:

Background

The molecular mechanisms underlying nonalcoholic fatty liver disease (NAFLD) remain to be fully elucidated. Ubiquitin specific protease 13 (USP13) is a critical participant in inflammation-related signaling pathways, which are linked to NAFLD. Herein, the roles of USP13 in NAFLD and the underlying mechanisms were investigated.

Methods

L02 cells and mouse primary hepatocytes were subjected to free fatty acid (FFA) to establish an in vitro model reflective of NAFLD. To prepare in vivo model of NAFLD, mice fed a high-fat diet (HFD) for 16 weeks and leptin-deficient (ob/ob) mice were used. USP13 overexpression and knockout (KO) strategies were employed to study the function of USP13 in NAFLD in mice.

Results

The expression of USP13 was markedly decreased in bot

SUBMITTER: Tang M 

PROVIDER: S-EPMC11264885 | biostudies-literature | 2024 Jul

REPOSITORIES: biostudies-literature