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Endothelial function-related targets refer to a heterogeneous group of molecular entities that maintain the physiological health and responsiveness of the vascular endothelium. Key members of this category include endothelial nitric oxide synthase (eNOS), which produces the potent vasodilator nitric oxide (NO), and G protein-coupled receptors like the endothelin receptors (ET-A and ET-B) that mediate vasoconstriction (Förstermann & Sessa, 2012; Gimbrone & García-Cardeña, 2016). The endothelium serves as a critical regulator of vascular tone, platelet aggregation, and leukocyte adhesion; thus, these targets are essential for preventing thrombosis and maintaining blood flow (Vanhoutte et al., 2009). Dysfunction in these targets is a primary pathological feature of cardiovascular diseases, including atherosclerosis and hypertension, often characterized by reduced NO bioavailability and increased oxidative stress. Pharmacological intervention typically involves drugs that either enhance protective pathways, such as statins and PDE5 inhibitors, or inhibit detrimental pathways, such as ACE inhibitors and endothelin receptor antagonists (StatPearls, 2023; PubChem). Monitoring endothelial function is clinically relevant, with flow-mediated dilation (FMD) serving as a non-invasive gold standard for assessing the integrated activity of these molecular targets in patients.
Modulation of nitric oxide (NO) bioavailability, inhibition of the renin-angiotensin-aldosterone system (RAAS), antagonism of endothelin receptors, and reduction of oxidative stress to restore vascular reactivity and endothelial integrity.
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