| Abstrakt: |
A study conducted by researchers at the University of Oklahoma Health Sciences Center explores the role of necroptosis, an inflammatory cell death pathway, in the progression of metabolic dysfunction-associated fatty liver disease (MAFLD). The study used a high-fat, high-fructose, high-cholesterol (HFHFrHC) mouse model of diet-induced MAFLD and targeted the mixed lineage kinase domain-like pseudokinase (MLKL), the terminal effector of necroptosis. The results showed that inhibiting necroptosis by targeting MLKL had tissue-specific effects on the liver and adipose tissue, and a dose-dependent effect on liver pathology. The study suggests that MLKL may play a role in diet-induced obesity, liver pathology, and insulin sensitivity. [Extracted from the article] |
