Inflammation in atherosclerosis: from theory to practice

Inflammation causes the formation, progression, and rupture of atherosclerotic plaques, which are an integral part of cardiovascular diseases. Numerous components are involved in the pathogenesis of atherosclerotic inflammation. Experimental studies have shown that the inflammatory subpopulation of monocytes / macrophages mainly accumulates in the atherosclerotic plaque and produces Pro-inflammatory cytokines that enhance atherogenesis. T-lymphocytes can contribute to the inflammatory processes that contribute to thrombosis by stimulating the production of collagen-destroying proteinases and a powerful procoagulant substance, tissue factor. Many research data link obesity, inflammation, and risk factors for atherosclerosis, which is a growing clinical concern given the increasing prevalence of obesity worldwide. Modulators of inflammation originating from visceral adipose tissue cause the liver to produce acute phase reagents involved in thrombosis. Additionally, levels of C-reactive protein increase with increasing levels of visceral adipose tissue. The adipose tissue of obese mice contains an increased number of macrophages and T-lymphocytes, increased activation of T-lymphocytes, and increased expression of interferon-gamma. It was found that interferon-gamma deficiency in mice reduces the production of inflammatory cytokines and the accumulation of inflammatory cells in adipose tissue. Another series of experiments on mice in vitro and in vivo confirmed that adiponectin, an adipocytokine whose plasma levels drop with obesity, acts as an endogenous anti-inflammatory modulator of both innate and acquired immunity in atherogenesis. Thus, the accumulation of experimental data confirms the key role of inflammation as a link between risk factors for atherosclerosis and the biology underlying the complications of this disease. A large Jupiter clinical trial confirms the clinical utility of assessing inflammatory status in therapeutic interventions to limit cardiovascular events. Thus, knowledge of the pathogenetic mechanisms underlying atherosclerotic inflammation is not only of theoretical value, but can also be used in practice when assessing the risk and prescribing therapy.