{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,30]],"date-time":"2026-09-30T16:42:13Z","timestamp":1790786533834,"version":"4.1.0"},"reference-count":50,"publisher":"American Diabetes Association","issue":"12","content-domain":{"domain":["diabetesjournals.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2014,12,1]]},"abstract":"<jats:p>Hyperhomocysteinemia (HHcy) is associated with increased diabetic cardiovascular diseases. However, the role of HHcy in atherogenesis associated with hyperglycemia (HG) remains unknown. To examine the role and mechanisms by which HHcy accelerates HG-induced atherosclerosis, we established an atherosclerosis-susceptible HHcy and HG mouse model. HHcy was established in mice deficient in cystathionine \u03b2-synthase (Cbs) in which the homocysteine (Hcy) level could be lowered by inducing transgenic human CBS (Tg-hCBS) using Zn supplementation. HG was induced by streptozotocin injection. Atherosclerosis was induced by crossing Tg-hCBS Cbs mice with apolipoprotein E-deficient (ApoE\u2212\/\u2212) mice and feeding them a high-fat diet for 2 weeks. We demonstrated that HHcy and HG accelerated atherosclerosis and increased lesion monocytes (MCs) and macrophages (M\u00d8s) and further increased inflammatory MC and M\u00d8 levels in peripheral tissues. Furthermore, Hcy-lowering reversed circulating mononuclear cells, MC, and inflammatory MC and MC-derived M\u00d8 levels. In addition, inflammatory MC correlated positively with plasma Hcy levels and negatively with plasma s-adenosylmethionine\u2013to\u2013s-adenosylhomocysteine ratios. Finally, l-Hcy and d-glucose promoted inflammatory MC differentiation in primary mouse splenocytes, which was reversed by adenoviral DNA methyltransferase-1. HHcy and HG, individually and synergistically, accelerated atherosclerosis and inflammatory MC and M\u00d8 differentiation, at least in part, via DNA hypomethylation.<\/jats:p>","DOI":"10.2337\/db14-0809","type":"journal-article","created":{"date-parts":[[2014,7,10]],"date-time":"2014-07-10T07:04:07Z","timestamp":1404975847000},"page":"4275-4290","update-policy":"https:\/\/doi.org\/10.2337\/ada-journal-policies","source":"Crossref","is-referenced-by-count":78,"title":["Hyperhomocysteinemia Potentiates Hyperglycemia-Induced Inflammatory Monocyte Differentiation and Atherosclerosis"],"prefix":"10.2337","volume":"63","author":[{"given":"Pu","family":"Fang","sequence":"first","affiliation":[{"name":"Center for Metabolic Disease Research, School of Medicine, Temple University, Philadelphia, PA"},{"name":"Department of Pharmacology, School of Medicine, Temple University, Philadelphia, PA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Daqing","family":"Zhang","sequence":"additional","affiliation":[{"name":"Center for Metabolic Disease Research, School of Medicine, Temple University, Philadelphia, PA"},{"name":"Department of Pharmacology, School of Medicine, Temple University, Philadelphia, PA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Zhongjian","family":"Cheng","sequence":"additional","affiliation":[{"name":"Center for Metabolic Disease Research, School of Medicine, Temple University, Philadelphia, PA"},{"name":"Department of Pharmacology, School of Medicine, Temple University, Philadelphia, PA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Chenghui","family":"Yan","sequence":"additional","affiliation":[{"name":"Cardiovascular Research Institute and Key Laboratory of Cardiology, Shenyang Northern Hospital, Shenyang, Liaoning, P.R. 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