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The bm12 Inducible Model of Systemic Lupus Erythematosus (SLE) in C57BL/6 Mice
Published on: November 1, 2015
Premature atherosclerotic cardiovascular disease and systemic lupus erythematosus from bedside to bench
1Rheumatology Division, University of Pennsylvania, Philadelphia, Pennsylvania, USA. vonfeldt@mail.med.upenn.edu
Insights
Systemic lupus erythematosus (SLE) significantly increases cardiovascular risk due to inflammation-driven atherosclerosis. Early endothelial dysfunction and vulnerable plaque are key factors in SLE patients, leading to premature cardiovascular events.
Area of Science:
- Rheumatology
- Cardiology
- Immunology
Background:
- Systemic lupus erythematosus (SLE) is an independent risk factor for cardiovascular events.
- Atherosclerotic plaque, not active vasculitis, is the primary cause of cardiovascular events in SLE patients.
- Inflammatory diseases like SLE are linked to vulnerable plaque rupture.
Purpose of the Study:
- To investigate the mechanisms underlying increased cardiovascular morbidity and mortality in SLE.
- To explore the role of endothelial dysfunction and inflammation in SLE-related atherosclerosis.
- To examine potential triggers like type I interferons in the atherosclerotic cascade.
Main Methods:
- Review of autopsy studies on coronary vessels in SLE patients.
- Analysis of associations between homocysteine levels and atherosclerotic plaque.
- Assessment of endothelial dysfunction in SLE vasculature.
- Exploration of preliminary evidence on type I interferons' role.
Main Results:
- SLE patients exhibit atherosclerotic plaque in coronary vessels.
- Elevated homocysteine levels correlate with atherosclerotic plaque presence and progression.
- Endothelial dysfunction is an early abnormality identified in SLE patients' vessels.
- Type I interferons may initiate atherosclerotic development via endothelial damage.
Conclusions:
- Premature cardiovascular disease in SLE is primarily driven by inflammation.
- Endothelial dysfunction and vulnerable plaque are critical factors in SLE cardiovascular events.
- Type I interferons represent a potential early trigger in SLE-associated atherosclerosis.
Abstract:
Cardiovascular morbidity and mortality in SLE is increased in patient with established disease, and SLE itself has been determined to be an independent risk factor for cardiovascular events. Autopsy studies have demonstrated that the coronary vessels of SLE patients have atherosclerotic plaque, and most cardiovascular events are not attributable to active vasculitis. It is believed that patients with inflammatory disease, including SLE, are more likely to have vulnerable plaque rupture, accounting for more frequent events. Elevated homocysteine levels have been associated with the presence and progression of atherosclerotic plaque. Enzyme polymorphisms involved in the folatehomocysteine pathway do not seem to contribute to differences in homocysteine concentration or atherosclerotic plaque. Recently, endothelial dysfunction has been identified as an early abnormality in ASCVD, and has been demonstrated in the vessels of SLE patients. Premature cardiovascular disease in SLE patients is likely attributable to the consequences of inflammation. There is preliminary evidence that type I interferons maybe the initial stimulation of the cascade of atherosclerotic development, starting with endothelial damage, and abnormal vascular repair.
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