The endothelin receptor type A (EDNRA) is a G protein-coupled receptor (GPCR) that binds endothelin-1 (ET-1), a potent vasoconstrictor peptide involved in cardiovascular homeostasis, cell proliferation, and tissue remodeling. EDNRA is primarily expressed in vascular smooth muscle cells, where it mediates vasoconstriction, inflammation, and fibrosis by activating signaling pathways such as phospholipase C and mitogen-activated protein kinase (MAPK). Dysregulation of EDNRA signaling has been implicated in hypertension, pulmonary arterial hypertension (PAH), cancer progression, and fibrotic diseases.
EDNRA antibodies are tools designed to detect, quantify, or inhibit this receptor in research and clinical contexts. In research, they aid in studying receptor localization, expression levels, and signaling mechanisms using techniques like immunohistochemistry, Western blotting, and flow cytometry. Therapeutically, EDNRA-targeting monoclonal antibodies or small-molecule antagonists (e.g., ambrisentan) have been explored to block pathogenic ET-1/EDNRA interactions, particularly in PAH and cancers where EDNRA overexpression correlates with tumor angiogenesis, metastasis, and poor prognosis.
Developing selective EDNRA antibodies remains challenging due to structural similarities with the endothelin receptor type B (EDNRB). However, advances in epitope mapping and antibody engineering have improved specificity, enabling more precise modulation of EDNRA for potential diagnostic and therapeutic applications.