Figure 1.

Endothelial dysfunction is regulated by different autocrine and paracrine factors released by endothelial cells. Different mediators are involved in the impairment of the vasoconstriction/vasodilation modulation: inhibition of eNOS through its dephosphorylation at Ser1177, which reduces NO release from ECs; downregulation of COX-2 and prostacyclin synthase, which are involved in PGI₂ synthesis from arachidonic acid; upregulation of COX-1 and thromboxane synthase, which increase TXA₂; and a decrease in EDHF release and reduction in ET-1 receptors on EC membranes are all factors that contribute to the contraction of the vessel walls. eNOS: endothelial nitric oxide synthase; NO: nitric oxide; EC: endothelial cells; VEGF: vascular endothelial growth factor; bFGF: basic fibroblast growth factor; COX: cyclooxygenase; PGI₂: prostacyclin; TXA₂: thromboxane A₂; EDHF: endothelium-derived hyperpolarizing factor; ET-1: endothelin-1. Image created with Biorender.com.