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Lipoprotein(a) Cellular Uptake Ex Vivo and Hepatic Capture In Vivo Is Insensitive to PCSK9 Inhibition With Alirocumab

Abstract : Lipoprotein(a) (Lp[a]) is the most common genetically inherited risk factor for cardiovascular disease. Many aspects of Lp(a) metabolism remain unknown. We assessed the uptake of fluorescent Lp(a) in primary human lymphocytes as well as Lp(a) hepatic capture in a mouse model in which endogenous hepatocytes have been ablated and replaced with human ones. Modulation of LDLR expression with the PCSK9 inhibitor alirocumab did not alter the cellular or the hepatic uptake of Lp(a), demonstrating that the LDL receptor is not a major route for Lp(a) plasma clearance. These results have clinical implications because they underpin why statins are not efficient at reducing Lp(a). (C) 2020 The Authors. Published by Elsevier on behalf of the American College of Cardiology Foundation.
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https://hal.inrae.fr/hal-03211827
Contributor : Pascal Lallemant <>
Submitted on : Thursday, April 29, 2021 - 12:22:23 PM
Last modification on : Sunday, May 9, 2021 - 4:36:14 PM

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Kévin Chemello, Sandra Beeské, Thi Thu Trang Tran, Valentin Blanchard, Elise Villard, et al.. Lipoprotein(a) Cellular Uptake Ex Vivo and Hepatic Capture In Vivo Is Insensitive to PCSK9 Inhibition With Alirocumab. JACC : Basic to Translational Science, Elsevier on behalf of the American College of Cardiology Foundation, 2020, 5 (6), pp.549-557. ⟨10.1016/j.jacbts.2020.03.008⟩. ⟨hal-03211827⟩

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