{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,2]],"date-time":"2026-07-02T17:32:52Z","timestamp":1783013572475,"version":"3.54.6"},"reference-count":55,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"12","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["ATVB"],"published-print":{"date-parts":[[2024,12]]},"abstract":"<jats:sec>\n            <jats:title>BACKGROUND:<\/jats:title>\n            <jats:p>Oxidative stress plays a crucial role in the pathogenesis of coronary artery disease. In cardiovascular research using murine models, the generation and maintenance of models with robust coronary arterial atherosclerosis has been challenging.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>METHODS:<\/jats:title>\n            <jats:p>\n              We characterized a new mouse model in which the last 3 amino acids of the carboxyl terminus of the HDL (high-density lipoprotein) receptor (SR-B1 [scavenger receptor, class B, type 1]) were deleted in a low-density lipoprotein receptor knockout (LDLR\n              <jats:sup>\u2212\/\u2212<\/jats:sup>\n              ) mouse model (SR-B1\u0394CT\/LDLR\n              <jats:sup>\u2212\/\u2212<\/jats:sup>\n              ) fed an atherogenic diet. We also tested the therapeutic effects of an oxidative stress-targeted nanoparticle in atherogenic diet\u2013fed SR-B1\u0394CT\/LDLR\n              <jats:sup>\u2212\/\u2212<\/jats:sup>\n              mice.\n            <\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>RESULTS:<\/jats:title>\n            <jats:p>\n              The SR-B1\u0394CT\/LDLR\n              <jats:sup>\u2212\/\u2212<\/jats:sup>\n              mice fed an atherogenic diet had occlusive coronary artery atherosclerosis, impaired cardiac function, and a dramatically lower survival rate, compared with LDLR\n              <jats:sup>\u2212\/\u2212<\/jats:sup>\n              mice fed the same diet. As SR-B1\u0394CT\/LDLR\n              <jats:sup>\u2212\/\u2212<\/jats:sup>\n              mice do not exhibit female infertility or low pup yield, they are far easier and less costly to use than the previously described SR-B1\u2013based models of coronary artery disease. We found that treatment with the targeted nanoparticles improved the cardiac functions and corrected hematologic abnormalities caused by the atherogenic diet in SR-B1\u0394CT\/LDLR\n              <jats:sup>\u2212\/\u2212<\/jats:sup>\n              mice but did not alter the distinctive plasma lipid levels.\n            <\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>CONCLUSIONS:<\/jats:title>\n            <jats:p>\n              The SR-B1\u0394CT\/LDLR\n              <jats:sup>\u2212\/\u2212<\/jats:sup>\n              mice developed diet-inducible, fatal atherosclerotic coronary artery disease, which could be ameliorated by targeted nanoparticle therapy. Our study provides new tools for the development of cardiovascular therapies.\n            <\/jats:p>\n          <\/jats:sec>","DOI":"10.1161\/atvbaha.124.321030","type":"journal-article","created":{"date-parts":[[2024,10,17]],"date-time":"2024-10-17T09:01:06Z","timestamp":1729155666000},"page":"2476-2488","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":6,"title":["Nanoparticle-Directed Antioxidant Therapy Can Ameliorate Disease Progression in a Novel, Diet-Inducible Model of Coronary Artery Disease"],"prefix":"10.1161","volume":"44","author":[{"given":"Shi","family":"Su","sequence":"first","affiliation":[{"name":"Cardiovascular Institute (S.S., Z.C., Q.K., P.M.K.), Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-1622-2105","authenticated-orcid":true,"given":"Zhifen","family":"Chen","sequence":"additional","affiliation":[{"name":"Cardiovascular Institute (S.S., Z.C., Q.K., P.M.K.), Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Qingen","family":"Ke","sequence":"additional","affiliation":[{"name":"Cardiovascular Institute (S.S., Z.C., Q.K., P.M.K.), Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0001-0686-9095","authenticated-orcid":true,"given":"Olivier","family":"Kocher","sequence":"additional","affiliation":[{"name":"Department of Pathology and Center for Vascular Biology Research (O.K.), Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, 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