Et1

ET-1, or endothelin-1, is a potent peptide produced primarily by vascular endothelial cells. It is synthesized as preproendothelin-1 and processed to big endothelin-1, which is cleaved by endothelin-converting enzyme to the active 21-amino-acid peptide ET-1. ET-1 exerts its effects by binding to endothelin receptors, mainly ETA and ETB, located on vascular smooth muscle cells and other tissues. The endothelin system also includes endothelin-2 and endothelin-3, contributing to local regulation of vascular tone and organ perfusion.

ET-1 plays a central role in controlling vascular tone and blood pressure and modulates renal sodium handling. It contributes to vascular remodeling and fibrotic processes in various organs. Dysregulation of the endothelin system is implicated in several diseases, including pulmonary arterial hypertension, systemic hypertension, heart failure, chronic kidney disease, and fibrotic disorders. Plasma ET-1 levels can reflect endothelial function and disease activity, though measurements depend on assay methodology and sample handling.

Clinically, endothelin receptor antagonists are used to counteract ET-1–mediated vasoconstriction. In pulmonary arterial hypertension, drugs such as bosentan, ambrisentan, and macitentan reduce pulmonary vascular resistance and improve exercise capacity, and they may be used in combination therapy. Potential adverse effects include liver injury, edema, and teratogenic risks, necessitating monitoring. Research continues into endothelin-converting enzyme inhibitors, receptor signaling modulators, and novel antagonists as therapies for cardiovascular, renal, and fibrotic diseases.

ET-1 is also studied as a biomarker and therapeutic target in oncology and inflammatory conditions, reflecting its broader role in vascular biology and tissue remodeling.