DDR2 ameliorates nonalcoholic hepatic steatosis by activating the AMPK/ACC pathway - PubMed
4 days ago
- #DDR2
- #AMPK/ACC pathway
- #MASLD
- DDR2 plays a role in ameliorating nonalcoholic hepatic steatosis by activating the AMPK/ACC pathway.
- Metabolic dysfunction-associated steatotic liver disease (MASLD) lacks effective drug treatments, making understanding its molecular mechanisms crucial.
- DDR2, a receptor tyrosine kinase, is involved in extracellular matrix remodeling, cell adhesion, and fibrosis, which are relevant to MASLD pathogenesis.
- Hepatic DDR2 expression is reduced in high-fat diet-fed and genetically obese mice (db/db mice).
- Overexpression of DDR2 reduces hepatic triglyceride accumulation and downregulates lipid synthesis-related genes in both cellular and animal models.
- DDR2 knockdown has the opposite effect, increasing lipid accumulation and related gene expression.
- Mechanistically, DDR2 enhances AMPK/ACC phosphorylation, suppressing hepatocyte lipogenesis.
- The study suggests DDR2 as a potential therapeutic target for MASLD management.