Related Experiment Video
Updated: Jan 13, 2026

Mouse Model of Metabolic Dysfunction-Associated Steatotic Liver Disease with Fibrosis
Published on: July 18, 2025
Acetyl-CoA-producing enzymes are a targetable metabolic entry point to MASLD and liver fibrosis
1Department of Hepatology and Gastroenterology, Charité - Universitätsmedizin Berlin, Campus Charité Mitte and Campus Virchow Klinikum, 13353 Berlin, Germany; Department of General, Visceral and Transplantation Surgery, Heidelberg University Hospital, 69120 Heidelberg, Germany.
Abstract:
Lipogenesis is one of the main drivers of metabolic dysfunction-associated steatotic liver disease (MASLD). The previewed work decreased acetyl-CoA by inhibiting ATP citrate lyase (ACLY) and acyl-CoA synthetase short-chain family member 2 (ACSS2) via EVT0185, thus inhibiting lipogenesis, hepatocyte metabolic stress, and hepatic stellate cell activation, reducing liver fibrosis.
Related Concept Videos
Overview of Fatty Acid Metabolism
Fatty acids are catabolized in a process called beta-oxidation, which takes place in the matrix of the mitochondria and converts their fatty acid chains into two-carbon units of acetyl groups. The acetyl...
Lipid Catabolism
Overview of Lipid Metabolism
Lipolysis: The Breakdown of Lipids:
Lipolysis is the process of breaking down lipids, particularly triglycerides, into glycerol and fatty acids. This process typically occurs in the adipose tissue and is triggered by various hormones, including glucagon and...

