IMMUNOPATHOGENESIS AND TREATMENT OF AUTOIMMUNE DISEASES: Edited by George C. TsokosThe latest in systemic lupus erythematosus-accelerated atherosclerosis: related mechanisms inform assessment and therapyAppleton, Brenna D.; Major, Amy S. Author Information aDepartment of Pathology, Microbiology and Immunology, Vanderbilt University bDepartment of Medicine, Division of Rheumatology and Immunology, Vanderbilt Medical Center cTennessee Valley Healthcare System, U.S. Department of Veterans Affairs, Nashville, Tennessee Correspondence to Amy S. Major, Vanderbilt University, 1161 21st Avenue South, A-3314 Medical Center North, Nashville, TN 37232, USA. Tel: +615 957 2496; e-mail: [email protected] Current Opinion in Rheumatology 33(2):p 211-218, March 2021. | DOI: 10.1097/BOR.0000000000000773 Buy Metrics Abstract Purpose of Review Accelerated atherosclerosis is a significant comorbidity and the leading cause of death for patients with systemic lupus erythematosus (SLE). It is now apparent that SLE-accelerated atherosclerosis is not driven solely by traditional cardiovascular risk factors, adding complexity to disease characterization and mechanistic understanding. In this review, we will summarize new insights into SLE-accelerated atherosclerosis evaluation, treatment, and mechanism. Recent findings Recent work highlights the need to incorporate inflammatory biomarkers into cardiovascular disease (CVD) risk assessments. This is especially true for SLE patients, in which mechanisms of immune dysfunction likely drive CVD progression. There is new evidence that commonly prescribed SLE therapeutics hinder atherosclerosis development. This effect is achieved both by reducing SLE-associated inflammation and by directly improving measures of atherosclerosis, emphasizing the interconnected mechanisms of the two conditions. Summary SLE-accelerated atherosclerosis is most likely the consequence of chronic autoimmune inflammation. Therefore, diligent management of atherosclerosis requires assessment of SLE disease activity as well as traditional cardiovascular risk factors. This supports why many of the therapeutics classically used to control SLE also modulate atherosclerosis development. Greater understanding of the mechanisms underlying this condition will allow for the development of more targeted therapeutics and improved outcomes for SLE patients. Copyright © 2020 Wolters Kluwer Health, Inc. All rights reserved.