Prostaglandin E receptor (EP receptor) (EP receptor)

Prostaglandin E receptors (EP receptors) are a family of four G protein-coupled receptors (EP1, EP2, EP3, and EP4) that mediate the physiological and pathological effects of Prostaglandin E2 (PGE2) and Prostaglandin E1 (PGE1) [1]. These receptors are involved in a wide array of biological processes, including the regulation of vascular tone, renal function, gastric mucosal protection, and the modulation of immune and inflammatory responses [2]. In the context of disease, the PGE2-EP receptor signaling axis is frequently hijacked; for instance, overstimulation of EP2 and EP4 receptors is associated with chronic inflammation and the progression of various cancers by promoting cell proliferation and immune evasion [4]. Therapeutic strategies targeting this system include direct receptor agonists for conditions like glaucoma or labor induction, and indirect modulation via nonsteroidal anti-inflammatory drugs (NSAIDs) that reduce ligand levels by inhibiting cyclooxygenase enzymes [3]. Direct antagonists, particularly for the EP4 subtype, are also being investigated for their potential in treating pain and enhancing cancer immunotherapy. However, systemic modulation of these receptors is often limited by safety concerns such as gastrointestinal ulceration, renal toxicity, and potential cardiovascular risks [3]. The complexity of the pathway arises from the distinct signaling cascades coupled to each receptor subtype, such as Gq for EP1, Gs for EP2 and EP4, and primarily Gi for EP3 [1].

Other names

Prostanoid EP receptorPGE receptorPTGEREP1-4

Direct agonism or antagonism of EP receptor subtypes (EP1-EP4) or indirect modulation of receptor activity by inhibiting cyclooxygenase enzymes (COX-1/COX-2) to reduce the synthesis of endogenous PGE1 and PGE2 ligands [1, 3].