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High-density lipoprotein functionality in systemic lupus erythematosus.

Shiva Ganjali1, Leila Shirmohammadi1, Morgayn I Read2

  • 1Department of Medical Biotechnology & Nanotechnology, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran.

Seminars in Arthritis and Rheumatism
|June 13, 2020
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Summary
This summary is machine-generated.

Systemic lupus erythematosus (SLE) patients face high cardiovascular disease risk due to inflammation-induced high-density lipoprotein (HDL) dysfunction. This review explores mechanisms behind altered HDL structure and function in SLE, contributing to atherosclerosis.

Keywords:
Anti-inflammatory activity, AutoimmunityCholesterol efflux capacityHDL functionalitySystemic lupus erythematosus

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Area of Science:

  • Immunology
  • Cardiovascular Medicine
  • Rheumatology

Background:

  • Systemic lupus erythematosus (SLE) is an autoimmune disease marked by inflammation, autoantibodies, and immune system overactivation.
  • SLE patients exhibit premature atherosclerosis and elevated mortality, despite advancements in treatment.
  • Traditional cardiovascular risk factors do not fully account for the heightened cardiovascular disease (CVD) risk in SLE.

Purpose of the Study:

  • To investigate the mechanisms underlying high-density lipoprotein (HDL) dysfunction in SLE patients.
  • To elucidate how inflammation in SLE alters HDL structure and function.
  • To identify specific molecular changes contributing to atherogenesis in SLE.

Main Methods:

  • Review of existing literature on SLE, atherosclerosis, and lipoprotein metabolism.
  • Analysis of studies investigating HDL components and functions in inflammatory conditions.
  • Examination of the impact of autoantibodies and immune complexes on endothelial cells and lipoproteins.

Main Results:

  • Inflammation in SLE is associated with altered lipoprotein metabolism, including increased atherogenic lipoproteins (LDL, VLDL) and decreased HDL-C.
  • Several factors contribute to decreased HDL levels and function in SLE, such as reduced apoA-I production, decreased LCAT activity, and increased SAA, endothelial lipase, and PLA2 activity.
  • Structural and functional changes in HDL during inflammation may play a role in CVD complications observed in SLE patients.

Conclusions:

  • HDL dysfunction is a significant factor contributing to the increased CVD risk in SLE patients.
  • Understanding the mechanisms of HDL dysfunction in SLE is crucial for developing targeted therapies.
  • Further research is needed to fully elucidate the complex interplay between SLE, inflammation, HDL, and atherosclerosis.