IL-1β in atherosclerotic vascular calcification: From bench to bedside

Abstract

Atherosclerotic vascular calcification contributes to increased risk of death in patients with cardiovascular diseases. Assessing the type and severity of inflammation is crucial in the treatment of numerous cardiovascular conditions. IL-1β, a potent proinflammatory cytokine, plays diverse roles in the pathogenesis of atherosclerotic vascular calcification. Several large-scale, population cohort trials have shown that the incidence of cardiovascular events is clinically reduced by the administration of anti-IL-1β therapy. Anti-IL-1β therapy might reduce the incidence of cardiovascular events by affecting atherosclerotic vascular calcification, but the mechanism underlying this effect remains unclear. In this review, we summarize current knowledge on the role of IL-1β in atherosclerotic vascular calcification, and describe the latest results reported in clinical trials evaluating anti-IL-1β therapies for the treatment of cardiovascular diseases. This review will aid in improving current understanding of the pathophysiological roles of IL-1β and mechanisms underlying its activity.

Dental Diseases Increase Risk of Aortic Arch Calcification Independent of Renal Dysfunction in Older Adults: Shenzhen Community Cohort Study

“…Inflammation is an important mechanism that promotes VC [30]. Inflammatory mediators, including interleukin-1β, interleukin-6, and tumor necrosis factor (TNF)-α, could stimulate the transformation of VSMCs from a contractile phenotype to an osteogenic phenotype [31,32]. Dental diseases are associated with a significant increase in the severity of systemic inflammation [33], which may be an important mechanism linking it with VC.…”

Mechanisms of Cardiovascular Calcification and Experimental Models: Impact of Vitamin K Antagonists

“…Inducing osteogenic differentiation in a subset of vascular cells is a fundamental biological process in atherosclerotic calcification, a very common form of vascular disease. The evolution of this process is regulated by specific inflammatory molecules, namely lipoproteins and cytokines, normally present in the atheromatous components of plaques [ 11 , 12 ]. Figure 1 describes the types, locations, and features of vascular calcification, along with associated clinical conditions.…”

Vascular calcification: Molecular mechanisms and therapeutic interventions

“…Therefore, recent scientific research has advanced the concept that chronic inflammation as a primary risk factor underlying aging and age‐related diseases 31 . Continuous upregulation of pro‐inflammatory cytokines (e.g., tumor necrosis factor alpha [TNF‐α], interleukin [IL]‐1β, IL‐6, cyclooxygenase [COX]‐2, inducible nitric oxide synthase) can activate the downstream inflammatory signaling pathways to promote the progression of diseases 32,33 . Previous studies have found that VC can be regulated by inflammation in myriad aspects.…”