A Role of IL-17 in Rheumatoid Arthritis Patients Complicated With Atherosclerosis

Abstract

Rheumatoid arthritis (RA) is mainly caused by joint inflammation. RA significantly increases the probability of cardiovascular disease. Although the progress of RA has been well controlled recently, the mortality of patients with RA complicated with cardiovascular disease is 1.5–3 times higher than that of patients with RA alone. The number of people with atherosclerosis in patients with RA is much higher than that in the general population, and atherosclerotic lesions develop more rapidly in patients with RA, which has become one of the primary factors resulting in the death of patients with RA. The rapid development of atherosclerosis in RA is induced by inflammation-related factors. Recent studies have reported that the expression of IL-17 is significantly upregulated in patients with RA and atherosclerosis. Simultaneously, there is evidence that IL-17 can regulate the proliferation, migration, and apoptosis of vascular endothelial cells and vascular smooth muscle cells through various ways and promote the secretion of several cytokines leading to the occurrence and development of atherosclerosis. Presently, there is no clear prevention or treatment plan for atherosclerosis in patients with RA. Therefore, this paper explores the mechanism of IL-17 in RA complicated with atherosclerosis and shows the reasons for the high incidence of atherosclerosis in patients with RA. It is hoped that the occurrence and development of atherosclerosis in patients with RA can be diagnosed or prevented in time in the early stage of lesions, and the prevention and treatment of cardiovascular complications in patients with RA can be enhanced to reduce mortality.

Stroke risk in rheumatoid arthritis patients: exploring connections and implications for patient care

“…Furthermore, RA is associated with accelerated atherosclerosis, an immune-mediated inflammatory process [ 28 ]. The systemic inflammation present in autoimmune diseases like RA [ 29 , 30 ] contributes to the progression of atherosclerosis. Endothelial dysfunction, which is an early pathological process in atherosclerosis, plays a significant role in the increased cardiovascular risk observed in systemic immune diseases, particularly RA.…”

Pro‐inflammatory cytokines mediating senescence of vascular endothelial cells in atherosclerosis

“…Studies have demonstrated that IL-17 is involved in the pathogenesis of AS [58,59]. IL-17 was highly expressed in atherosclerotic plaques, and the levels of serum IL-17 in patients with AS were significantly higher than those in healthy subjects [34,[60][61][62]. Recently, Li et al reported that IL-17 induced the senescence of VECs [44].…”

The forgotten key players in rheumatoid arthritis: IL-8 and IL-17 – Unmet needs and therapeutic perspectives

“…Within its biological effects, IL-17A might promote accelerated atherosclerosis, which is a key extra-articular manifestation of RA ( 73 ). The observation that in the ApoE −/− (apolipoprotein E-deficient) mouse model, which is a model prone to accelerated atherosclerosis, IL-17A blockage reduced the plaque burden, IL-6 levels, G-CSF levels, CXCL1 expression, and macrophage content in the aorta strongly suggests, among many others, a pathogenetic role of IL-17A in the atherogenic process ( 74 ).…”