MiR-33 deletion in hepatocytes attenuates MASLD-MASH-HCC progression.

ABSTRACT: The complexity of the mechanisms underlying metabolic dysfunction-associated steatotic liver disease (MASLD) progression remains a significant challenge for the development of effective therapeutics. miRNAs have shown great promise as regulators of biological processes and as therapeutic targets for complex diseases. Here, we study the role of hepatic miR-33, an important regulator of lipid metabolism, during the progression of MASLD and the development of hepatocellular carcinoma (HCC). We report that miR-33 was elevated in the livers of humans and mice with MASLD and that its deletion in hepatocytes (miR-33 HKO) improved multiple aspects of the disease, including steatosis and inflammation, limiting the progression to metabolic dysfunction-associated steatotic hepatitis (MASH), fibrosis,

SUBMITTER: Fernandez-Tussy P 

PROVIDER: S-EPMC11466198 | biostudies-literature | 2024 Aug

REPOSITORIES: biostudies-literature