Impact of subclinical inflammatory markers on the development of cardiovascular pathology in patients with the metabolic syndrome

Metabolic syndrome currently remains one of the most pressing problems in medicine, since it makes its decisive contribution to the development of cardiovascular diseases and cerebral complications. Another important problem of modern medicine is arterial hypertension, which is one of the constituent criteria of metabolic syndrome, whose mechanism of development is due to a disruption in the work of the renin-angiotensin-aldosterone system, the sympathoadrenal system, an increased content of pro-inflammatory cytokines, as well as an imbalance in the adipokine system. Adipose tissue now acts not just as a structure that provides our body with energy only, but now it acts as an organ of the endocrine system, producing a large number of metabolically active substances. Patients with metabolic syndrome have been found to have elevated levels of proinflammatory cytokines were increased: monocytic chemotactic protein-1 (MCP-1), interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α). These cytokines are thought to be synthesised by adipose tissue macrophages and are involved in the pathogenesis of the metabolic syndrome. Oxidative stress can induce insulin resistance in adipocytes. The pathogenesis of oxidative stress in adipocytes in MS is still a mystery. This knowledge would be very useful in developing new approaches to MS therapy. Given the significant effect of chemokines in MS on the development of systemic inflammation, insulin resistance, and arterial hypertension, scientists have an important task not only to describe the actions of individual chemokines in hypertension, but also to characterize how the effect on one chemokine modulates the expression and/or function of other chemokines and their related receptors.