Systemic lupus erythematosus and cardiovascular disease
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Updated: Jul 5, 2026

The bm12 Inducible Model of Systemic Lupus Erythematosus (SLE) in C57BL/6 Mice
Published on: November 1, 2015
1Department of Rheumatology, Karolinska University Hospital, Huddinge, Sweden. johan.frostegard@ki.se
Insights
Systemic lupus erythematosus (SLE) significantly increases cardiovascular disease (CVD) risk due to traditional and non-traditional factors. Atherosclerosis in SLE may be more prone to rupture, necessitating close monitoring of all risk factors for CVD prevention.
Area of Science:
- Immunology
- Cardiology
- Rheumatology
Background:
- Atherosclerosis, an inflammatory arterial disease, is the primary cause of cardiovascular disease (CVD).
- Systemic lupus erythematosus (SLE) patients face a substantially elevated risk of CVD, making SLE-related atherosclerosis a critical clinical concern.
- Immune system dysregulation in SLE may offer insights into general CVD mechanisms.
Purpose of the Study:
- To investigate the interplay of traditional and non-traditional risk factors contributing to CVD in SLE patients.
- To explore the potential for heightened atherosclerotic lesion vulnerability in SLE compared to non-SLE atherosclerosis.
- To emphasize the clinical importance of monitoring CVD risk in SLE management.
Main Methods:
- Review and synthesis of existing research on CVD risk factors in SLE.
- Analysis of traditional CVD risk factors (dyslipidemia, hypertension, renal disease) in the context of SLE.
- Examination of non-traditional risk factors, including inflammation and antiphospholipid antibodies (aPL), and their association with CVD in SLE.
Main Results:
- CVD risk in SLE is driven by a combination of traditional and non-traditional factors acting synergistically.
- Non-traditional factors such as inflammation, dyslipidemia (high triglycerides), hypertension, renal disease, antiphospholipid antibodies (aPL), and oxidized low-density lipoprotein (LDL) are linked to CVD in SLE.
- Atherothrombosis is a key mechanism, and pro-inflammatory reactions or prothrombotic factors like aPL may increase atherosclerotic plaque rupture risk in SLE.
Conclusions:
- Premature atherosclerosis may be a feature in SLE, though it might affect specific patient subgroups.
- Comprehensive CVD risk management in SLE requires vigilant monitoring of both traditional and non-traditional risk factors.
- Understanding the unique atherosclerotic profile in SLE is crucial for effective CVD prevention and treatment strategies.
Abstract:
Atherosclerosis is an inflammatory disease characterised by presence of activated immune competent cells in middle-sized and large arteries and is the major cause of cardiovascular disease (CVD). The risk of CVD is very high in systemic lupus erythematosus (SLE). SLE-related CVD and atherosclerosis are, therefore, important clinical problems but may in addition also have implications for the role of immune reactions in CVD in general. Others and we have recently demonstrated that risk factors for CVD in SLE are both traditional and non-traditional acting in concert. Traditional risk factors implicated in SLE include, for example, dyslipidemia (especially high triglycerides), hypertension, renal disease, non-traditional as inflammation, antiphospholipid antibodies (aPL) and low-density lipoprotein (LDL) oxidation are also associated with CVD in SLE. Atherothrombosis is likely to be a major underlying mechanism and is not only an increased risk of thrombosis per se. It is possible that factors like proinflammatory reactions or prothrombotic factors, such as aPL, make atherosclerotic lesions in SLE more prone to rupture than in 'normal' atherosclerosis. Whether premature atherosclerosis is a general feature of SLE or only affects a subgroup of patients is presently not clear. Treatment of patients with SLE should include a close monitoring of traditional risk factors and also the above-mentioned non-traditional for CVD.
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