{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,23]],"date-time":"2026-09-23T18:59:20Z","timestamp":1790189960188,"version":"4.1.0"},"reference-count":70,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"10","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["ATVB"],"published-print":{"date-parts":[[2026,10]]},"abstract":"<jats:sec>\n                    <jats:title>BACKGROUND:<\/jats:title>\n                    <jats:p>Reverse cholesterol transport by HDLs (high-density lipoproteins) is considered an antiatherogenic metabolic pathway. Hepatocytes are the main contributors to the efficacy of this pathway by the production of apoA-I (apolipoprotein A1) and its lipidation by ABCA1 (ATP-binding cassette transporter A1), selective uptake of cholesterol via SR-BI (scavenger receptor class B type 1), and uptake of entire HDL particles. The molecular determinants of the latter step are not well understood.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>METHODS:<\/jats:title>\n                    <jats:p>We performed a genome-wide RNA interference screen for genes limiting the uptake of HDL fluorescently labeled at its protein moiety into Huh-7 hepatocarcinoma cells. Top hit genes were validated by targeted in vitro experiments and the analysis of associations between their variants and HDL-C (HDL-cholesterol) levels in the databases of the Global Lipids Genetics Consortium and the UK Biobank, as well as inborn errors of metabolism and their respective mouse models.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>RESULTS:<\/jats:title>\n                    <jats:p>\n                      The knockdown of 128 genes significantly inhibited HDL uptake. Six of them encode components of the COPI (coat protein I) coatomer, namely,\n                      <jats:italic toggle=\"yes\">COPA<\/jats:italic>\n                      ,\n                      <jats:italic toggle=\"yes\">COPB1<\/jats:italic>\n                      ,\n                      <jats:italic toggle=\"yes\">COPB2<\/jats:italic>\n                      ,\n                      <jats:italic toggle=\"yes\">COPG1<\/jats:italic>\n                      ,\n                      <jats:italic toggle=\"yes\">ARCN1<\/jats:italic>\n                      , and\n                      <jats:italic toggle=\"yes\">COPZ1<\/jats:italic>\n                      . Knocking down any of them decreased the uptake of both fluorescently labeled proteins and lipids of HDL, the cell surface abundance of SR-BI, and\n                      <jats:italic toggle=\"yes\">APOA1<\/jats:italic>\n                      expression and apoA-I secretion but increased the cell surface abundance of ABCA1. Common single-nucleotide polymorphisms of\n                      <jats:italic toggle=\"yes\">ARCN1<\/jats:italic>\n                      and\n                      <jats:italic toggle=\"yes\">COPB1<\/jats:italic>\n                      were associated with significantly higher HDL-C levels in the population, while rare\n                      <jats:italic toggle=\"yes\">COPA<\/jats:italic>\n                      and\n                      <jats:italic toggle=\"yes\">COPG1<\/jats:italic>\n                      variants causing immunopathies were associated with rather lower levels of HDL-C in both affected patients and the corresponding genetically modified mice.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>CONCLUSIONS:<\/jats:title>\n                    <jats:p>In hepatocytes, the COPI coatomer regulates HDL holoparticle uptake, selective lipid uptake, apoA-I secretion, and ABCA1 expression, and thereby, it influences plasma levels of HDL-C.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1161\/atvbaha.126.324616","type":"journal-article","created":{"date-parts":[[2026,8,13]],"date-time":"2026-08-13T09:00:15Z","timestamp":1786611615000},"update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":1,"title":["COPI Coatomer Regulates Several Steps of HDL Metabolism"],"prefix":"10.1161","volume":"46","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-7672-7623","authenticated-orcid":true,"given":"Grigorios","family":"Panteloglou","sequence":"first","affiliation":[{"name":"Institute for Clinical Chemistry (G.P., P.Z., M.Y., S.K., A.P., E.S., S.R., S.H., J.R., L.R., A.v.E.), University of Z\u00fcrich and University Hospital Z\u00fcrich, Switzerland."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Paolo","family":"Zanoni","sequence":"additional","affiliation":[{"name":"Institute for Clinical Chemistry (G.P., P.Z., M.Y., S.K., A.P., E.S., S.R., S.H., J.R., L.R., A.v.E.), University of Z\u00fcrich and University Hospital Z\u00fcrich, Switzerland."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0005-4516-3844","authenticated-orcid":true,"given":"Christopher S.","family":"Law","sequence":"additional","affiliation":[{"name":"Cardiovascular Research Institute, University of California, San Francisco (C.S.L., A.K.S.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-4363-4444","authenticated-orcid":true,"given":"Brian","family":"Woods","sequence":"additional","affiliation":[{"name":"Division of Immunology, Boston Children\u2019s Hospital, Harvard Medical School, MA (B.W., J.C., R.S.G.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-0092-5594","authenticated-orcid":true,"given":"Alaa","family":"Othman","sequence":"additional","affiliation":[{"name":"Institute of Molecular Systems Biology (A.O.), ETH Z\u00fcrich, Switzerland."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-2199-0886","authenticated-orcid":true,"given":"Mustafa","family":"Yalcinkaya","sequence":"additional","affiliation":[{"name":"Institute for Clinical Chemistry (G.P., P.Z., M.Y., S.K., A.P., E.S., S.R., S.H., J.R., L.R., A.v.E.), University of Z\u00fcrich and University Hospital Z\u00fcrich, Switzerland."},{"name":"Now with Division of Molecular Medicine, Department of Medicine, Columbia University, New York, NY (M.Y.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-8302-526X","authenticated-orcid":true,"given":"Simon F.","family":"Norrelykke","sequence":"additional","affiliation":[{"name":"Scientific Center for Optical and Electron Microscopy (S.F.N., A.J.R., S.S., M. 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