{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,2]],"date-time":"2026-05-02T05:36:16Z","timestamp":1777700176947,"version":"3.51.4"},"reference-count":49,"publisher":"IMR Press","issue":"4","license":[{"start":{"date-parts":[[2026,4,23]],"date-time":"2026-04-23T00:00:00Z","timestamp":1776902400000},"content-version":"unspecified","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Front. Biosci. (Landmark Ed)"],"abstract":"<jats:p>Background: The significance of cholesterol efflux as a predictor of coronary artery disease (CAD) remains controversial. The intracellular cholesterol export via the ABCA1 transporter involves the acceptance of cholesterol by both lipid-free apolipoprotein A-I and high-density lipoproteins (HDL). An estimate of the efficiencies of two reactions is thus required. Methods: HDL from the plasma of 63 control and 76 male CAD patients was obtained by the precipitation of apoB-containing lipoproteins and denatured by urea. We measured apoA-I dissociation concomitant with HDL denaturation by agarose gel electrophoresis followed by immunodetection and the expression of 65 preselected genes in blood mononuclear cells by real-time PCR. The total cholesterol efflux capacity (CEC) of ATP-binding cassette transporter A1 (ABCA1)-mediated cholesterol efflux from RAW 264.7 macrophages, when pre\u03b2-HDL and \u03b1-HDL act as competitive inhibitors of each other for the binding to ABCA1 transporter, was measured with intact HDL and pre-denatured HDL as a source of lipid-free apoA-I. Results: The phospholipid:apoA-I and cholesterol:apoA-I ratios in HDL from CAD patients were higher than those for control patients across the full range of plasma HDL-cholesterol levels. ApoA-I partitioned 1.5-fold higher into the water phase for HDL from CAD patients relative to controls. In CAD patients, the dissociation parameter D was inversely correlated with absolute and normalized per apoA-I phospholipid and cholesterol levels in HDL. For control patients, the D parameter was positively correlated with ABCA1 gene expression. For CAD patients, the D parameter was positively correlated with PLTP and inversely with CUBN and ALB gene expression. ApoA-I functionality in ABCA1-mediated cholesterol efflux from RAW 264.7 macrophages to lipid-free apoA-I generated from urea-induced HDL denaturation was similar for HDL from control and CAD groups. The retained CEC of lipid-free apoA-I in CAD may be masked by competition with \u03b1-HDL, which has a lower CEC, for ABCA1 binding to pre\u03b2-HDL. Conclusions: The enrichment of HDL with cholesterol and phospholipids may contribute to the increased apoA-I dissociation from HDL in CAD. Estimates of both lipid-free apoA-I and intact HDL may be a prerequisites for a detailed study of ABCA1-mediated cholesterol efflux, which could allow these apoA-I forms to be identified as CAD predictors.<\/jats:p>","DOI":"10.31083\/fbl50403","type":"journal-article","created":{"date-parts":[[2026,4,29]],"date-time":"2026-04-29T09:29:27Z","timestamp":1777454967000},"source":"Crossref","is-referenced-by-count":0,"title":["ApoA-I Dissociated From Human HDL Retains its Acceptor Properties in ABCA1-mediated Cholesterol Efflux From RAW 264.7 Macrophages in Coronary Artery Disease"],"prefix":"10.31083","volume":"31","author":[{"given":"Veronika B.","family":"Baserova","sequence":"first","affiliation":[{"name":"Laboratory of Structural Fundamentals of Lipoprotein Metabolism, National Medical Research Center for Therapy and Preventive Medicine, 101990 Moscow, Russia"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Mikhail A.","family":"Popov","sequence":"additional","affiliation":[{"name":"Cardiosurgery Department, M.F. Vladimirsky Moscow Regional Research and Clinical Institute MONIKI, 129090 Moscow, Russia"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-0781-9890","authenticated-orcid":true,"given":"Alexander D.","family":"Dergunov","sequence":"additional","affiliation":[{"name":"Laboratory of Structural Fundamentals of Lipoprotein Metabolism, National Medical Research Center for Therapy and Preventive Medicine, 101990 Moscow, Russia"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"16242","published-online":{"date-parts":[[2026,4,23]]},"reference":[{"key":"ref1","doi-asserted-by":"publisher","unstructured":"Rohatgi A, Khera A, Berry JD, Givens EG, Ayers CR, Wedin KE, et al. HDL cholesterol efflux capacity and incident cardiovascular events. The New England Journal of Medicine. 2014; 371: 2383\u20132393.","DOI":"10.1056\/NEJMoa1409065"},{"key":"ref2","doi-asserted-by":"publisher","unstructured":"Dergunov AD, Baserova VB. 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