ArticleMolecular and cellular biochemistry2026
The METTL3/TRIM37 axis contributes to the progression of non-alcoholic fatty liver disease by promoting CAV1 degradation.
Article in Molecular and cellular biochemistry, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Caveolin-1 (CAV1), a principal structural component of caveolae, plays a pivotal role in the regulation of lipid metabolism, signal transduction, and cellular homeostasis. Dysregulation of CAV1 has been implicated in the pathogenesis of metabolic diseases, particularly non-alcoholic fatty liver disease (NAFLD). However, the precise molecular mechanisms responsible for CAV1 in NAFLD remain largely unclear. In vitro experiments were performed using THLE-3 or HepG2 cells treated with palmitic acid (PA) to establish a lipotoxic model. Quantitative real-time polymerase chain reaction was used to detect mRNA levels, whereas western blotting was performed to analyze protein expression. Cell viability, proliferation, apoptosis, and lipid deposition were assessed using Cell Counting Kit-8 (CCK-8), 5-ethynyl-2'-deoxyuridine (EdU), flow cytometry, and Oil Red O staining, respectively. Ferroptosis was evaluated by measuring Fe
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