Interaction of interleukin-6 and angiotensin II in atherosclerosis: culprit for inflammation?

Atherosclerosis is a chronic inflammatory disease perpetuated by a variety of pro-inflammatory mediators. Fatal outcomes of this disease, which include myocardial infarction, stroke, and sudden death, remain the major cause of morbidity and mortality in industrialized countries. Accumulated evidence obtained from pathological observations, state-of-the-art imaging, and large-scale clinical trials showed that these fatal events are mainly the results of pathological vascular remodeling processes, suggesting a close interaction between inflammation, vascular remodeling, and the renin-angiotensin system. The Heart Outcomes and Prevention Evaluation (HOPE) study demonstrated that the renin-angiotensin system blockade reduces fatal and nonfatal clinical ischaemic events in high-risk patients, which further implicate the renin-angiotensin system in plaque development and stability. Since experimental and clinical evidence point to inflammatory mediators such as interferon-γ, interleukin-1β, interleukin-18, and interleukin-10 as well as interleukin-6 as promoters/predictors of cardiovascular events, this paper discusses the clinical basis and the potential molecular and cellular interactions between the RAS and cytokines and their potential impact on remodeling processes at the atherosclerotic plaques.