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- W2023986039 abstract "Hyperlipidemia is a well-recognized risk factor for atherosclerosis and can be regulated by adipokines. Expression of the adipokine resistin-like molecule alpha (Retnla) is regulated by food intake; whether Retnla has a role in the pathogenesis of hyperlipidemia and atherosclerosis is unknown. Here we report that Retnla has a cholesterol-lowering effect and protects against atherosclerosis in low-density lipoprotein receptor-deficient mice. On a high-fat diet, Retnla deficiency promotes hypercholesterolaemia and atherosclerosis, whereas Retnla overexpression reverses these effects and improves the serum lipoprotein profile, with decreased cholesterol in the very low-density lipoprotein fraction concomitant with reduced serum apolipoprotein B levels. We show that Retnla upregulates cholesterol-7-α-hydroxylase, a key hepatic enzyme in the cholesterol catabolic pathway, through induction of its transcriptional activator liver receptor homologue-1, leading to increased excretion of cholesterol in the form of bile acids. These findings define Retnla as a novel therapeutic target for treating hypercholesterolaemia and atherosclerosis." @default.
- W2023986039 created "2016-06-24" @default.
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- W2023986039 date "2014-07-15" @default.
- W2023986039 modified "2023-10-03" @default.
- W2023986039 title "The adipokine Retnla modulates cholesterol homeostasis in hyperlipidemic mice" @default.
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- W2023986039 doi "https://doi.org/10.1038/ncomms5410" @default.
- W2023986039 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/25022542" @default.
- W2023986039 hasPublicationYear "2014" @default.
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