Key result
Chemokines and their receptors drive vascular inflammation in hypertension, highlighting pathways beyond standard blood pressure control.
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Hypertension is a major risk factor for cardiovascular disease, which is a serious health problem in the highly industrialized countries. In more than 95% of the cases, the etiology of hypertension remains unknown. A key role in the etiology of hypertension is played by endothelial dysfunction and the inflammatory reaction in the vascular wall, in which the low molecular weight proteins so called chemokines are involved. The chemokines involved in the pathogenesis of hypertension include monocyte chemoattractant protein-1, MCP-1, CCL2, interferon-inducible protein (IP-10; CXCL10), interleukin-8 (IL-8; CXCL8), RANTES (CCL5), fractalkine (CX3CL1) and their receptors CCR2, CCR5, CXCR1, CXCR2, CXCR3 and CX3CR1. The mechanisms involving chemokines and their receptors in the pathogenesis of hypertension are complex and not fully understood. They include the impact of the migration of macrophages and monocytes to the vascular wall, endothelial dysfunction, effects on nitric oxide and endothelin-1 and smooth muscle cell proliferation. Chemokines are also involved in the pathogenesis of complications of hypertension, such as atherosclerosis, myocardial and renal fibrosis. In Poland, only about 26% of patients are effectively treated with antihypertensive drugs. The use of new therapeutic methods based on the inhibition of the inflammatory process in the vascular wall, including the impact on the function of chemokines and their receptors, could improve the effectiveness of the treatment of hypertension.
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Martynowicz et al. (2014) conducted a review in Hypertension. Chemokines and their receptors was evaluated. Chemokines and their receptors drive vascular inflammation in hypertension, where etiology is unknown in >95% of cases and only ~26% of patients in Poland are effectively treated.
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