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Systemic Lupus Erythematosus and Endothelial Dysfunction: A Close Relationship
Edoardo Sciatti1, Ilaria Cavazzana2, Enrico Vizzardi1
1Cardiology Unit, University and ASST Spedali Civili, Brescia, Italy.
Insights
Systemic lupus erythematosus (SLE) patients experience accelerated atherosclerosis due to endothelial dysfunction, increasing cardiovascular disease risk. Early assessment and management of cardiovascular risk factors are crucial for these patients.
Area of Science:
- Cardiovascular Medicine
- Rheumatology
- Immunology
Background:
- Systemic lupus erythematosus (SLE) is associated with a 6-fold higher incidence of accelerated atherosclerosis compared to the general population.
- Accelerated atherosclerosis in SLE stems from complex interactions involving classical and non-classical cardiovascular risk factors.
- Endothelial dysfunction and arterial stiffness are linked to subclinical and widespread atherosclerosis in SLE patients.
Purpose of the Study:
- To review and analyze the association between systemic lupus erythematosus (SLE) and endothelial dysfunction.
- To explore the mechanisms contributing to endothelial dysfunction in SLE.
Main Methods:
- Literature review and meta-analysis of studies investigating SLE and atherosclerosis.
- Analysis of proposed mechanisms for endothelial dysfunction in SLE, including immune cell activation and inflammatory markers.
Main Results:
- Studies indicate a significant prevalence of subclinical accelerated atherosclerosis in SLE patients from childhood compared to controls.
- Endothelial dysfunction is a key feature contributing to increased cardiovascular risk in SLE.
Conclusions:
- Endothelial dysfunction in SLE is multifactorial, involving impaired apoptotic cell clearance, oxidative stress, autoantibodies, T cell subtypes, and cytokine cascades.
- Multidisciplinary management is recommended for early assessment and periodic treatment of cardiovascular risk factors in SLE patients.
- Further prospective studies are required to validate the benefits of proposed management strategies.
Background:
Accelerated atherosclerosis, responsible for premature cardiovascular disease, has been estimated to develop or progress in 10% of systemic lupus erythematosus (SLE) patients each year and to be 6-fold more frequent in SLE compared with the general population. The mechanisms underlying accelerated atherosclerosis in SLE are complex and involve classical and "non-classical" cardiovascular risk factors. Subclinical and disseminated atherosclerosis is associated with endothelial dysfunction and arterial stiffness.
Objective:
The aim of this review is to analyze the association between SLE and endothelial dysfunction.
Results And Conclusion:
Different mechanisms have been proposed to explain the prevalence of endothelial dysfunction in SLE, which are briefly reported in this review: impaired clearance of apoptotic cells, oxidative stress markers, B cell activation with different circulating autoantibodies, different subtypes of T lymphocytes, cytokine cascade. Several studies and meta-analyses show a significant trend towards a prevalence of subclinical accelerated atherosclerosis in patients with SLE compared with healthy controls, since childhood. Based on general considerations, we suggest a multidisciplinary management to assess endothelial dysfunction at the diagnosis of the disease and to periodically search for and treat the traditional cardiovascular risk factors. Prospective studies are needed to confirm the benefits of this management.
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