{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,1,3]],"date-time":"2026-01-03T04:36:28Z","timestamp":1767414988194,"version":"build-2065373602"},"reference-count":135,"publisher":"MDPI AG","issue":"9","license":[{"start":{"date-parts":[[2021,5,6]],"date-time":"2021-05-06T00:00:00Z","timestamp":1620259200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/100010551","name":"Texas Heart Institute","doi-asserted-by":"publisher","award":["765-64050"],"award-info":[{"award-number":["765-64050"]}],"id":[{"id":"10.13039\/100010551","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100004663","name":"Ministry of Science and Technology, Taiwan","doi-asserted-by":"publisher","award":["MOST 107-2314-B-039-053-MY3"],"award-info":[{"award-number":["MOST 107-2314-B-039-053-MY3"]}],"id":[{"id":"10.13039\/501100004663","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100004587","name":"Instituto de Salud Carlos III","doi-asserted-by":"publisher","award":["PI16\/00471"],"award-info":[{"award-number":["PI16\/00471"]}],"id":[{"id":"10.13039\/501100004587","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["JCM"],"abstract":"<jats:p>Atherosclerosis has been linked with an increased risk of atherosclerotic cardiovascular disease (ASCVD). Autoimmune rheumatic diseases (AIRDs) are associated with accelerated atherosclerosis and ASCVD. However, the mechanisms underlying the high ASCVD burden in patients with AIRDs cannot be explained only by conventional risk factors despite disease-specific factors and chronic inflammation. Nevertheless, the normal levels of plasma low-density lipoprotein (LDL) cholesterol observed in most patients with AIRDs do not exclude the possibility of increased LDL atherogenicity. By using anion-exchange chromatography, human LDL can be divided into five increasingly electronegative subfractions, L1 to L5, or into electropositive and electronegative counterparts, LDL (+) and LDL (\u2212). Electronegative L5 and LDL (\u2212) have similar chemical compositions and can induce adverse inflammatory reactions in vascular cells. Notably, the percentage of L5 or LDL (\u2212) in total LDL is increased in normolipidemic patients with AIRDs. Electronegative L5 and LDL (\u2212) are not recognized by the normal LDL receptor but instead signal through the lectin-like oxidized LDL receptor 1 (LOX-1) to activate inflammasomes involving interleukin 1\u03b2 (IL-1\u03b2). Here, we describe the detailed mechanisms of AIRD-related ASCVD mediated by L5 or LDL (\u2212) and discuss the potential targeting of LOX-1 or IL-1\u03b2 signaling as new therapeutic modalities for these diseases.<\/jats:p>","DOI":"10.3390\/jcm10091992","type":"journal-article","created":{"date-parts":[[2021,5,6]],"date-time":"2021-05-06T11:10:27Z","timestamp":1620299427000},"page":"1992","update-policy":"https:\/\/doi.org\/10.3390\/mdpi_crossmark_policy","source":"Crossref","is-referenced-by-count":10,"title":["Autoimmune Rheumatic Diseases: An Update on the Role of Atherogenic Electronegative LDL and Potential Therapeutic Strategies"],"prefix":"10.3390","volume":"10","author":[{"given":"Der-Yuan","family":"Chen","sequence":"first","affiliation":[{"name":"Translational Medicine Center, China Medical University Hospital, Taichung 404, Taiwan"},{"name":"Rheumatology and Immunology Center, China Medical University Hospital, Taichung 404, Taiwan"},{"name":"College of Medicine, China Medical University, Taichung 404, Taiwan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Tatsuya","family":"Sawamura","sequence":"additional","affiliation":[{"name":"Department of Molecular Pathophysiology, Shinshu University School of Medicine, Matsumoto 390-8621, Japan"},{"name":"Department of Life Innovation, Institute for Biomedical Sciences, Shinshu University, Matsumoto 390-8621, Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Richard A. F.","family":"Dixon","sequence":"additional","affiliation":[{"name":"Molecular Cardiology Research Laboratories, Texas Heart Institute, Houston, TX 77030, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-0224-591X","authenticated-orcid":false,"given":"Jos\u00e9 Luis","family":"S\u00e1nchez-Quesada","sequence":"additional","affiliation":[{"name":"Cardiovascular Biochemistry Group, Biomedical Research Institute IIB Sant Pau, 08041 Barcelona, Spain"},{"name":"CIBER of Diabetes and Metabolic Diseases (CIBERDEM), 08041 Barcelona, Spain"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Chu-Huang","family":"Chen","sequence":"additional","affiliation":[{"name":"Department of Life Innovation, Institute for Biomedical Sciences, Shinshu University, Matsumoto 390-8621, Japan"},{"name":"Vascular and Medicinal Research, Texas Heart Institute, Houston, TX 77030, USA"},{"name":"New York Heart Research Foundation, Mineola, NY 11501, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"1968","published-online":{"date-parts":[[2021,5,6]]},"reference":[{"key":"ref_1","doi-asserted-by":"crossref","first-page":"2045","DOI":"10.1161\/ATVBAHA.108.179705","article-title":"Inflammation in Atherosclerosis","volume":"32","author":"Libby","year":"2012","journal-title":"Arter. 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