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Update on cardiovascular disease in lupus
Laura B Lewandowski1, Mariana J Kaplan
1Systemic Autoimmunity Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, Maryland, USA.
Insights
Systemic lupus erythematosus (SLE) patients face high cardiovascular disease risk due to immune system dysregulation accelerating atherosclerosis. Understanding these immune pathways offers new therapeutic targets for improved patient outcomes.
Area of Science:
- Immunology
- Cardiovascular Science
- Rheumatology
Background:
- Atherosclerotic cardiovascular disease (ASCVD) causes significant mortality in systemic lupus erythematosus (SLE) patients.
- Traditional cardiovascular risk factors do not fully explain the elevated ASCVD risk in SLE.
- Emerging immunologic pathways in SLE are implicated in accelerated atherosclerosis.
Purpose of the Study:
- To review the immunologic underpinnings of accelerated atherosclerosis in SLE.
- To identify how aberrant immune responses in SLE contribute to cardiovascular disease.
- To highlight potential therapeutic targets for managing ASCVD in SLE patients.
Main Methods:
- Review of recent immunologic discoveries related to SLE and atherosclerosis.
- Analysis of innate and adaptive immune responses in lupus pathogenesis.
- Examination of specific cellular and molecular pathways involved in endothelial dysfunction and plaque progression.
Main Results:
- Aberrant immune responses in SLE, including defective apoptosis and dysregulated type I interferon, contribute to endothelial dysfunction.
- SLE macrophages exhibit an inflammatory phenotype that promotes atherosclerotic plaque progression.
- Autoantibodies, abnormal lipoprotein function, and neutrophil responses are implicated.
Conclusions:
- Immune dysregulation in SLE plays a critical role in accelerated atherosclerosis.
- Targeting specific immune pathways may reduce cardiovascular risk and improve outcomes in SLE patients.
- Further research into the immunology of ASCVD in SLE is warranted for developing novel therapies.
Purpose Of Review:
Atherosclerotic cardiovascular disease confers significant morbidity and mortality in patients with systemic lupus erythematosus (SLE) and cannot be fully explained by traditional cardiovascular risk factors. Recent immunologic discoveries have outlined putative pathways in SLE that may also accelerate the development of atherosclerosis.
Recent Findings:
Aberrant innate and adaptive immune responses implicated in lupus pathogenesis may also contribute to the development of accelerated atherosclerosis in these patients. Defective apoptosis, abnormal lipoprotein function, autoantibodies, aberrant neutrophil responses, and a dysregulated type I interferon pathway likely contribute to endothelial dysfunction. SLE macrophages have an inflammatory phenotype that may drive progression of plaque.
Summary:
Recent discoveries have placed increased emphasis on the immunology of atherosclerotic cardiovascular disease. Understanding the factors that drive the increased risk for cardiovascular disease in SLE patients may provide selective therapeutic targets for reducing inflammation and improving outcomes in atherosclerosis.
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