{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,8]],"date-time":"2026-10-08T03:02:42Z","timestamp":1791428562926,"version":"4.3.3"},"reference-count":123,"publisher":"Bioscientifica","issue":"1","license":[{"start":{"date-parts":[[2024,1,1]],"date-time":"2024-01-01T00:00:00Z","timestamp":1704067200000},"content-version":"unspecified","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["vb.bioscientifica.com"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2024,3,1]]},"abstract":"<jats:p>\n                    Cardiovascular disease, the primary cause of human mortality globally, is predominantly caused by a progressive disorder known as atherosclerosis. Atherosclerosis refers to the process of accumulation of cholesterol-enriched lipoproteins and the concomitant initiation of inflammatory processes in the arterial wall, including the recruitment of immune cells. This leads to the formation of atherosclerotic plaques, initially causing a thickening of the arterial wall and narrowing of arteries. However, as plaque formation progresses, atherosclerotic plaques may become unstable and rupture, leading to a blood clot that blocks the affected artery or travels through the blood to block blood flow elsewhere. In the early 1990s, emerging gene editing methods enabled the development of apolipoprotein E knockout (\n                    <jats:italic>\n                      Apoe\n                      <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    <\/jats:italic>\n                    ) and low-density lipoprotein receptor knockout (\n                    <jats:italic>\n                      Ldlr\n                      <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    <\/jats:italic>\n                    ) mice. These mice have been instrumental in unraveling the complex pathogenesis of atherosclerosis. Around the same time, human\n                    <jats:italic>APOE*3-Leiden<\/jats:italic>\n                    transgenic mice were generated, which were more recently cross-bred with human cholesteryl ester transfer protein (CETP) transgenic mice to generate\n                    <jats:italic>APOE*3-Leiden.CETP<\/jats:italic>\n                    mice. This model appears to closely mimic human lipoprotein metabolism and responds to classic lipid-lowering interventions due to an intact ApoE\u2013LDLR pathway of lipoprotein remnant clearance. In this review, we describe the role of lipid metabolism and inflammation in atherosclerosis development and highlight the characteristics of the frequently used animal models to study atherosclerosis, with a focus on mouse models, discussing their advantages and limitations. Moreover, we present a detailed methodology to quantify atherosclerotic lesion area within the aortic root region of the murine heart, as well as details required for scoring atherosclerotic lesion severity based on guidelines of the American Heart Association adapted for mice.\n                  <\/jats:p>","DOI":"10.1530\/vb-23-0017","type":"journal-article","created":{"date-parts":[[2024,3,1]],"date-time":"2024-03-01T09:59:47Z","timestamp":1709287187000},"update-policy":"https:\/\/doi.org\/10.1530\/crossmarkpolicy-12","source":"Crossref","is-referenced-by-count":12,"title":["Atherosclerosis: an overview of mouse models and a detailed methodology to quantify lesions in the aortic root"],"prefix":"10.1530","volume":"6","author":[{"ORCID":"https:\/\/orcid.org\/0009-0006-3794-0364","authenticated-orcid":true,"given":"Jamie I","family":"van der Vaart","sequence":"first","affiliation":[{"name":"Division of Endocrinology, Department of Medicine, Leiden University Medical Center, Leiden, The Netherlands"},{"name":"Einthoven Laboratory for Vascular and Regenerative Medicine, Leiden University Medical Center, Leiden, The Netherlands"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-2637-3801","authenticated-orcid":true,"given":"Robin","family":"van Eenige","sequence":"additional","affiliation":[{"name":"Division of Endocrinology, Department of Medicine, Leiden University Medical Center, Leiden, The Netherlands"},{"name":"Einthoven Laboratory for Vascular and Regenerative Medicine, Leiden University Medical Center, Leiden, The Netherlands"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Patrick C N","family":"Rensen","sequence":"additional","affiliation":[{"name":"Division of Endocrinology, Department of Medicine, Leiden University Medical Center, Leiden, The Netherlands"},{"name":"Einthoven Laboratory for Vascular and Regenerative Medicine, Leiden University Medical Center, Leiden, The Netherlands"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sander","family":"Kooijman","sequence":"additional","affiliation":[{"name":"Division of Endocrinology, Department of Medicine, Leiden University Medical Center, Leiden, The Netherlands"},{"name":"Einthoven Laboratory for Vascular and Regenerative Medicine, Leiden University Medical Center, Leiden, The Netherlands"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"416","reference":[{"key":"bib1","series-title":"Journal of the American College of Cardiology","first-page":"2982","article-title":"Global burden of cardiovascular diseases and risk factors, 1990\u20132019: update from the GBD 2019 study","volume":"76","author":"Roth","year":"2020","unstructured":"Roth GAMensah GAJohnson COAddolorato GAmmirati EBaddour LMBarengo NCBeaton AZBenjamin EJBenziger CP, et al.Global burden of cardiovascular diseases and risk factors, 1990\u20132019: update from the GBD 2019 study. 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