It is demonstrated that chemerin stimulates SMC proliferation and migration via autophagy, which may lead to vascular structural remodeling in metabolic hypertension.
We previously demonstrated primed platelet-derived growth factor receptor β<sup>+</sup> (PDGFR-β<sup>+</sup>)/smooth muscle cell (SMC) marker<sup>+</sup> progenitors at the muscular-unmuscular arteriole border in the normal lung, and in hypoxia-induced pulmonary hypertension, a single primed cell migrates distally and expands clonally, giving rise to most of the pathological smooth muscle coating of small arterioles.
Results indicated that stretching aortic segments to higher than optimal preload depolarizes the SMC and causes Ca<sup>2+</sup> unloading of the contractile SR, making them extremely sensitive to small changes in the basal release of NO from EC as can occur in hypertension or arterial stiffening.
Indeed, recent advances in understanding the molecular basis of vascular dysfunction point towards a reduction of sarcoplasmic reticulum Ca2+ uptake and an impairment of Ca2+ cycling in vascular EC and SMC from patients and preclinical models with cardiac diseases or with cardiovascular risk factors such as diabetes, hypercholesterolemia, coronary artery diseases, as well as other conditions such as pulmonary hypertension.