Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD) Mouse Model (Gene-editing)

The production and clearance of fat in liver cells is regulated by a variety of genes - of which, mutation, deletion, overexpression, or modification may affect fat metabolism, thereby forming fatty liver. Human genes associated with MASLD pathologies can be replicated across species by targeting analogous genes to develop this specific MASLD animal model.

1. Pten Gene Knockout Mice

Phosphatase and tensin homolog (PTEN) is a lipid phosphatase involved in the fatty acid β-oxidation (FAO) of hepatic cells and triacylglycerol synthesis, which also plays the role as a negative regulator in signaling pathways such as apoptosis, cell proliferation and differentiation, and tumor formation. One study found that liver damage discovered in liver tissue-specific Pten gene knockout mice is similar to that of human MASH. Such mice can successively develop steatohepatitis, liver fibrosis, and liver adenoma within 10 weeks of age, with up to 66% of the cohort pathology complicated with HCC.

2. Apoe Gene Knockout Mice

Apoe (apolipoprotein E) gene knockout (KO) mice are commonly used in atherosclerosis (AS) studies. Interestingly, Apoe KO mice which are fed a high-fat, high-cholesterol diet can develop metabolic dysfunction-associated steatohepatitis (MASH) phenotypes, such as steatosis, inflammation, and fibrosis.

Detection Items: Body weight, food intake, serum biochemical test (alanine aminotransferase, aspartate aminotransferase, serum total cholesterol, triglyceride content, etc.), pathological analysis of liver tissue (liver tissue H&E staining, oil red).

3. Other Genetically Modified Mouse Models Related to Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD) Research