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Journal of Lipid Research
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    • Research Article
      Open Access

      Antisense oligonucleotide–mediated inhibition of angiopoietin-like protein 3 increases reverse cholesterol transport in mice

      Journal of Lipid Research
      Vol. 62100101Published online: August 5, 2021
      • Thomas A. Bell III
      • Mingxia Liu
      • Aaron J. Donner
      • Richard G. Lee
      • Adam E. Mullick
      • Rosanne M. Crooke
      Cited in Scopus: 0
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        Supported by an abundance of experimental and genetic evidence, angiopoietin-like protein 3 (ANGPTL3) has emerged as a promising therapeutic target for cardiovascular disease. ANGPTL3 is primarily produced by the liver and is a potent modulator of plasma lipids and lipoproteins. Experimental models and subjects with loss-of-function Angptl3 mutations typically present with lower levels of HDL-C than noncarriers. The effect of ANGPTL3 on HDL-C is typically attributed to its function as an inhibitor of the enzyme endothelial lipase.
        Antisense oligonucleotide–mediated inhibition of angiopoietin-like protein 3 increases reverse cholesterol transport in mice
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