Ednra, or endothelin receptor type A, is a key receptor involved in multiple physiological processes. It binds to endothelin-1, a potent vasoconstrictor, and is part of pathways related to vasoregulation, cell proliferation, and migration. Dysregulation of the Ednra-mediated signaling pathway has implications for various diseases, highlighting its biological importance. Mouse models with Ednra mutations have been valuable for studying its functions [10].

In multiple myeloma, EDNRA-expressing mesenchymal cells expand in the interstitial bone marrow and are associated with disease progression. High EDNRA expression is linked to increased angiogenesis and disrupted vasculature [1]. In colorectal cancer, EDNRA promotes cancer progression through the EDN1/EDNRA/β -arrestin axis, regulating STAT3 phosphorylation. Pharmacological intervention of this pathway may be a potential treatment [2]. Additionally, in kidney disease, activation of ETA (Ednra) by endothelin causes vasoconstriction and kidney damage, and endothelin receptor antagonists are being explored as a treatment strategy [3]. Polymorphisms in EDNRA are associated with intracerebral hemorrhage, large artery atherosclerotic stroke, and intracranial aneurysm, affecting disease susceptibility [4,5,7,9]. In cancer immunotherapy, EDNRA expression is related to immune infiltration, prognosis, and response to immunotherapy, and may be a target for tumour immunotherapy [6]. Hydroxytyrosol can decrease EDNRA expression through epigenetic modification in colorectal cancer cells [8].

In conclusion, Ednra is a crucial receptor involved in vasoregulation and various disease-related processes such as cancer progression, kidney disease, and cerebrovascular diseases. Studies using mouse models and human genetic analysis have enhanced our understanding of Ednra's functions, which may provide new directions for disease treatment and prevention in these areas.