Endothelin-1 receptor

Endothelin refers to a family of potent 21-amino acid vasoactive peptides, the most prominent of which is endothelin-1, secreted primarily by endothelial cells. These peptides function via two main G protein-coupled receptors: endothelin receptor type A (ET_A/EDNRA), predominantly mediating vasoconstriction and pathological proliferation, and endothelin receptor type B (ET_B/EDNRB), which generally promotes vasodilation, ET-1 clearance, and other protective effects. Endothelin signaling is essential in maintaining vascular homeostasis but, when dysregulated, is implicated in hypertension, cardiovascular diseases, pulmonary arterial hypertension, fibrosis, and cancer. Multiple antagonists targeting these receptors are clinically approved, primarily for pulmonary arterial hypertension. The term "endothelin" itself is ambiguous for drug discovery; it is crucial to specify either the particular ligand (e.g., endothelin-1) or a receptor subtype (ET_A or ET_B) given their different druggability profiles and physiological roles[1][2][3][5][6][7][8]. Note: For structured data or drug discovery purposes, clarify whether the molecular target is the ligand (e.g., endothelin-1) or the receptor (ET_A/ET_B). Current query refers broadly to the whole system, not a single gene/protein.

Other names

Endothelins (for the peptide family)ET-1, ET-2, ET-3 (isoforms)Endothelin-1 (most prominent ligand)Endothelin receptor (for the family of GPCRs: ET_A/EDNRA and ET_B/EDNRB)Endothelin system

Antagonists block binding of endogenous endothelin ligands (primarily ET-1) to ET_A and/or ET_B receptors, reducing vasoconstriction, cell proliferation, and fibrosis. - Agonists (rarely used therapeutically) stimulate ET_B receptor functions (e.g., vasodilation, clearance of ET-1)[1][3][5][7]