ArticleLipids in health and disease2026
SiRNA-based inactivation of Angptl3 alleviates high-fat diet-induced MAFLD and atherosclerosis in LDLR-deficient hamsters.
Article in Lipids in health and disease, 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
backgroundAngiopoietin-like protein 3 (Angptl3), a factor secreted by the liver, inhibits lipoprotein lipase and other lipases by forming a complex with Angptl4 and 8. However, whether inhibition of Angptl3 can alleviate hepatic lipid accumulation and atherosclerosis remains unclear. Therefore, this study explored the effect of small interfering RNA (siRNA)-based inactivation of Angptl3 on metabolic dysfunction-associated fatty liver disease (MAFLD) and atherosclerosis in male LDLR-deficient hamsters.
methodsRecombinant adeno-associated virus serotype 9 (AAV9) encoding Angptl3-siRNA or empty AAV (AAV9-null) were injected into male 4-month-old LDLR−/− hamsters via the jugular vein. Subsequently, all hamsters were administered with a 16-week high-fat diet (HFD) feeding to induce atherosclerosis. RT-PCR and pathological analysis were used to investigate the mechanism of hepatic lipid accumulation and detect atherosclerotic plaque formation in the heart and aorta.
resultsOn HFD, Angptl3-siRNA-treated hamsters displayed significantly decreased plasma triglyceride (TG), total cholesterol, high-density lipoprotein-cholesterol, and glucose levels, compared with the AAV9-null hamsters. FPLC analysis further revealed a marked reduction of TG and cholesterol contents in VLDL/LDL fractions. Plasma apolipoprotein analysis showed relatively lower ApoB/ApoE levels and higher ApoA1 levels. Moreover, Angptl3-siRNA markedly accelerated the clearance of triglyceride-rich lipoproteins in LDLR−/− hamsters. Consistently, results from hepatic lipid extraction, Oil Red O and Sirius Red staining demonstrated that Angptl3-siRNA reduced hepatic lipid accumulation and ameliorated HFD-induced MAFLD. RT-PCR revealed a dramatic decrease in the expression of Acc1, Fasn, Srebp1c, Cd36, Fatp1, Tgfβ, Cd68, Tnfa, and Col1a1 as well as a marked increase in Abcg5, Abcg8, Ppara, and Cpt1 expression, which participated in fatty acid synthesis and oxidation, cholesterol synthesis and efflux, inflammation and fibrosis. Pathological analysis indicated that Angptl3-siRNA attenuated the formation of atherosclerotic plaques in the aortic root and aorta when compared with the control group.
conclusionsThese findings demonstrated that siRNA-based inactivation of Angptl3 alleviated MAFLD and atherosclerosis induced by HFD in LDLR−/− hamsters, which further confirmed that inhibition of Angptl3 may provide a novel therapeutic approach for atherosclerosis by reducing hyperlipidemia and hepatic lipid accumulation.
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