The role of inflammatory biomarkers in the arterial hypertension

Abstract

Studies on both humans and animals have found evidence of a link between inflammation and hypertension (HTN). A lower serum calprotectin level was found to be independently related to HTN. The elevated ferritin–HTN link could be mediated by fatty liver disease and insulin resistance (IR). Similarly, fibrinogen was engaged in several processes that may increase the risk of HTN which including hemostasis, coagulation, and the proliferation of smooth muscle cells in the artery wall, and others. Procalcitonin monitoring could be a useful biomarker in inflammation related to atherosclerosis and early-stage HTN. Plasminogen activator 1 (PAI-1) was not just a result of HTN but also contributes to its development. Also, the positive correlation between monocyte chemoattractant protein 1 (MCP-1) levels with blood pressure were found among smokers. The high level of pentraxin 3 (PTX3) was one of the factors of increased blood pressure. Galectin 3 (Gal-3) may contribute to the onset and progression of diastolic dysfunction-complicated HTN. Increased intercellular adhesion molecules (ICAM)/vascular cell adhesion molecule 1 (VCAM-1) ligand expression, along with a drop in soluble cell adhesion molecules (sCAMs) and endocan, points to endothelium deactivation with lower blood pressure, which reduces the adherence of circulatory leukocytes to endothelium and, as a result, lowers the probability of atherosclerosis developing. The circulating levels of soluble VCAM-1 were substantially connected with left ventricular mass indexes (LVMIs) and were higher in uncomplicated essential hypertension (EH) patients with left ventricle (LV) hypertrophy than in those without LV hypertrophy.