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• W2803642149 abstract "Background and aimsObesity, hepatosteatosis, and hypertriglyceridemia are components of the metabolic syndrome and independent risk factors for cardiovascular disease. The lipid droplet-associated protein CIDEC (cell death-inducing DFFA-like effector C), known in mice as FSP27 (fat-specific protein 27), plays a key role in maintaining triacylglyceride (TAG) homeostasis in adipose tissue and liver, and controls circulating TAG levels in mice. Importantly, mutations and SNPs in CIDEC are associated with dyslipidemia and altered metabolic function in humans. Here we tested whether systemic silencing of Fsp27 using antisense oligonucleotides (ASOs) was atheroprotective in LDL receptor knock-out (Ldlr–/–) mice.MethodsAtheroprone Ldlr–/– mice were fed a high-fat, high-cholesterol diet for 12 weeks while simultaneously dosed with saline, ASO-ctrl, or ASO-Fsp27.ResultsData show that, compared to control treatments, silencing Fsp27 significantly reduced body weight gain and visceral adiposity, prevented diet-induced hypertriglyceridemia, and reduced atherosclerotic lesion size both in en face aortas and in the aortic root.ConclusionsOur findings suggest that therapeutic silencing of Fsp27 with ASOs may be beneficial in the prevention and management of atherogenic disease in patients with metabolic syndrome." @default.
• W2803642149 created "2018-06-01" @default.
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• W2803642149 date "2018-08-01" @default.
• W2803642149 modified "2023-09-26" @default.
• W2803642149 title "Therapeutic silencing of FSP27 reduces the progression of atherosclerosis in Ldlr–/– mice" @default.
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• W2803642149 doi "https://doi.org/10.1016/j.atherosclerosis.2018.05.045" @default.
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