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The coronary endothelium is a specialized monolayer of cells lining the interior surface of coronary blood vessels, serving as a critical interface between circulating blood and the vessel wall (StatPearls, 2023) [1]. It functions as a dynamic endocrine and paracrine organ, regulating vascular tone, blood flow, and platelet aggregation through the synthesis and release of factors like nitric oxide, prostacyclin, and endothelin-1 (PubMed, 2021) [2]. Endothelial dysfunction, characterized by impaired vasodilation and a pro-inflammatory state, is a primary precursor to atherosclerosis and coronary artery disease (NIH, 2022) [3]. Therapeutic intervention often focuses on restoring endothelial health or mitigating the effects of its dysfunction to prevent myocardial ischemia and infarction (Journal of the American College of Cardiology, 2020) [4]. Although it is a tissue rather than a single molecular target, it contains various receptors and enzymes that are the focus of treatments using statins, ACE inhibitors, and vasodilators (Nature Reviews Cardiology, 2019) [5].
Drugs targeting the coronary endothelium typically act by modulating the production or activity of endothelial-derived factors, such as increasing nitric oxide bioavailability or inhibiting the renin-angiotensin-aldosterone system (StatPearls, 2023) [1].
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