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We examine how chronic systemic inflammation modifies the lipoprotein profile toward a pro-oxidant state, characterized by dysfunctional HDL and elevated oxidized LDL. Central to this vascular pathology are type I interferon-driven cascades, excessive neutrophil extracellular trap release, and biased macrophage polarization toward pro-atherogenic phenotypes. Furthermore, the roles of pathogenic autoantibodies, genetic susceptibility, and the metabolic impact of specific immunosuppressants are explored. Integrating these mechanistic insights is essential for refining cardiovascular risk assessment and identifying novel immunomodulatory interventions. Ultimately, understanding the unique SLE\u2013atherosclerosis axis provides a foundation for reducing cardiovascular morbidity and improving long-term outcomes in this vulnerable population.<\/jats:p>","DOI":"10.3389\/fimmu.2026.1818480","type":"journal-article","created":{"date-parts":[[2026,4,22]],"date-time":"2026-04-22T05:50:20Z","timestamp":1776837020000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":1,"title":["Systemic lupus erythematosus\u2013accelerated atherosclerosis: mechanistic insights and clinical implications"],"prefix":"10.3389","volume":"17","author":[{"given":"Dexiu","family":"Li","sequence":"first","affiliation":[{"name":"Xiyuan Hospital, China Academy of Chinese Medical Sciences","place":["Beijing, China"]},{"name":"National Clinical Research Center for Chinese Medicine Cardiology","place":["Beijing, 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