ArticleFrontiers in cardiovascular medicine2022
Vascular Inflammation in Mouse Models of Systemic Lupus Erythematosus.
Article in Frontiers in cardiovascular medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 6 citations in OpenAlex.
- Immunopathogenesis of accelerated atherosclerosis in systemic lupus erythematosus: from innate and adaptive dysregulation to clinical implications.Frontiers in immunology · 2026Review
- A Novel Preclinical Murine Model of Systemic Lupus Erythematosus-Like Cardiovascular Disease.ACR open rheumatology · 2024Article
- The Aconitate Decarboxylase 1/Itaconate Pathway Modulates Immune Dysregulation and Associates with Cardiovascular Disease Markers and Disease Activity in Systemic Lupus Erythematosus.Journal of immunology (Baltimore, Md. : 1950) · 2024Article
- The aconitate decarboxylase 1/itaconate pathway modulates immune dysregulation and associates with cardiovascular disease markers in SLE.medRxiv : the preprint server for health sciences · 2024Article
- TLR7 Activation Accelerates Cardiovascular Pathology in a Mouse Model of Lupus.Frontiers in immunology · 2022Article
- Saponins fromFrontiers in pharmacology · 2022Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Vascular inflammation mediated by overly activated immune cells is a significant cause of morbidity and mortality in systemic lupus erythematosus (SLE). Several mouse models to study the pathogenesis of SLE are currently in use, many of which have different mechanisms of pathogenesis. The diversity of these models allows interrogation of different aspects of the disease pathogenesis. To better determine the mechanisms by which vascular inflammation occurs in SLE, and to assist future researchers in choosing the most appropriate mouse models to study cardiovascular complications in SLE, we suggest that direct comparisons of vascular inflammation should be conducted among different murine SLE models. We also propose the use of
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