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High‐Density Lipoprotein in Lupus: Disease Biomarkers and Potential Therapeutic Strategy
Author(s) -
Kim Sang Yeop,
Yu Minzhi,
Morin Emily E.,
Kang Jukyung,
Kaplan Mariana J.,
Schwendeman Anna
Publication year - 2020
Publication title -
arthritis and rheumatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.106
H-Index - 314
eISSN - 2326-5205
pISSN - 2326-5191
DOI - 10.1002/art.41059
Subject(s) - inflammation , systemic lupus erythematosus , medicine , proinflammatory cytokine , high density lipoprotein , biomarker , oxidative stress , reverse cholesterol transport , dysfunctional family , disease , immunology , systemic inflammation , lipoprotein , cholesterol , biology , biochemistry , clinical psychology
Systemic lupus erythematosus ( SLE ) patients exhibit accelerated development of atherosclerosis and increased incidents of cardiovascular disease ( CVD ) that cannot be explained by traditional risk factors alone. Accumulating evidence suggests that reduced levels of high‐density lipoproteins ( HDL s), along with altered HDL composition and function, may contribute to the accelerated atherosclerosis in SLE patients. Normally, HDL s play various atheroprotective roles through facilitating cholesterol efflux, inhibiting vascular inflammation, and scavenging oxidative species. However, systemic inflammation, oxidative stress, and autoimmunity in SLE patients induce changes in HDL size distribution and proteomic and lipidomic signatures. These compositional changes in HDL s result in the formation of proinflammatory, dysfunctional HDL . These lupus‐altered HDL s have impaired antiatherogenic function with reduced cholesterol efflux capacities, impaired antioxidation abilities, and diminished antiinflammatory properties. In fact, dysfunctional HDL may promote atherogenesis by inducing inflammation. Thus, dysfunctional HDL s could be an important biomarker of accelerated atherosclerosis in lupus. Additionally, HDL ‐targeted therapies, especially infusion of reconstituted HDL s, may serve as a potential therapeutic intervention for SLE patients with CVD .