Salusins: Potential Use as a Biomarker for Atherosclerotic Cardiovascular Diseases

Abstract

Human salusin-αand salusin-βare related peptides produced from prosalusin. Bolus injection of salusin-βinto rats induces more profound hypotension and bradycardia than salusin-α. Central administration of salusin-βincreases blood pressure via release of norepinephrine and arginine-vasopressin. Circulating levels of salusin-αand salusin-βare lower in patients with essential hypertension. Salusin-βexerts more potent mitogenic effects on human vascular smooth muscle cells (VSMCs) and fibroblasts than salusin-α. Salusin-βaccelerates inflammatory responses in human endothelial cells and monocyte-endothelial adhesion. Human macrophage foam cell formation is stimulated by salusin-βbut suppressed by salusin-α. Chronic salusin-βinfusion into apolipoprotein E-deficient mice enhances atherosclerotic lesions; salusin-αinfusion reduces lesions. Salusin-βis expressed in proliferative neointimal lesions of porcine coronary arteries after stenting. Salusin-αand salusin-βimmunoreactivity have been detected in human coronary atherosclerotic plaques, with dominance of salusin-βin macrophage foam cells, VSMCs, and fibroblasts. Circulating salusin-βlevels increase and salusin-αlevels decrease in patients with coronary artery disease. These findings suggest that salusin-βand salusin-αmay contribute to proatherogenesis and antiatherogenesis, respectively. Increased salusin-βand/or decreased salusin-αlevels in circulating blood and vascular tissue are closely linked with atherosclerosis. Salusin-αand salusin-βcould be candidate biomarkers and therapeutic targets for atherosclerotic cardiovascular diseases.