title: The human prostacyclin receptor from structure function to disease.
abstract: Thirty years have passed since Vane and colleagues first described a substance, prostanoid X, from microsomal fractions (later called prostacyclin) that relaxed rather than contracted mesenteric arteries. The critical role of prostacyclin in many pathophysiological conditions, such as atherothrombosis, has only recently become appreciated (through receptor knockout mice studies, selective cyclooxygenase-2 inhibition clinical trials, and the discovery of dysfunctional prostacyclin receptor genetic variants). Additionally, important roles in such diverse areas as pain and inflammation, and parturition are being uncovered. Prostacyclin-based therapies, currently used for pulmonary hypertension, are accordingly emerging as possible treatments for such diseases, fueling interests in structure function studies for the receptor and signal transduction pathways in native cells. The coming decade is likely to yield many further exciting advances.
authors.affiliation: Department of Pharmacology and Toxicology, Dartmouth Medical School, Hanover, New Hampshire 03755, USA.
authors.forename: Kathleen A
authors.initials: KA
authors.lastname: Martin
authors.forename: Scott
authors.initials: S
authors.lastname: Gleim
authors.forename: Larkin
authors.initials: L
authors.lastname: Elderon
authors.forename: Kristina
authors.initials: K
authors.lastname: Fetalvero
authors.forename: John
authors.initials: J
authors.lastname: Hwa
mesh_terms: D000818:Animals; D004194:Disease; D011464:Epoprostenol; D014644:Genetic Variation; D006801:Humans; D044006:Receptors, Epoprostenol / Q000737:chemistry* / Q000235:genetics / Q000378:metabolism*; D013329:Structure-Activity Relationship
chemical_list: D044006:Receptors, Epoprostenol; D011464:Epoprostenol