ReviewAccelerated vascular disease in systemic lupus erythematosus: Role of macrophage

- Accelerated atherosclerosis is a serious health problem for patients with SLE.
- Macrophages play a role in tissue remodeling including plaque formation and rupture.
- Macrophages release factors that accelerate development of atherosclerosis in SLE.
- Extrinsic factors can control macrophage behavior in SLE.
- Measuring and targeting sphingolipids in SLE can be a novel approach to therapy.

Atherosclerosis is a chronic inflammatory condition that is considered a major cause of death worldwide. Striking phenomena of atherosclerosis associated with systemic lupus erythematosus (SLE) is its high incidence in young patients. Macrophages are heterogeneous cells that differentiate from hematopoietic progenitors and reside in different tissues to preserve tissue integrity. Macrophages scavenge modified lipids and play a major role in the development of atherosclerosis. When activated, macrophages secret inflammatory cytokines. This activation triggers apoptosis of cells in the vicinity of macrophages. As such, macrophages play a significant role in tissue remodeling including atherosclerotic plaque formation and rupture. In spite of studies carried on identifying the role of macrophages in atherosclerosis, this role has not been studied thoroughly in SLE-associated atherosclerosis. In this review, we address factors released by macrophages as well as extrinsic factors that may control macrophage behavior and their effect on accelerated development of atherosclerosis in SLE.