Prostacyclin analogs as the brakes for pulmonary artery smooth muscle cell proliferation: is it sufficient to treat severe pulmonary hypertension?
Tuder
Rubin M
RM
Division of Cardiopulmonary Pathology, Department of Pathology, The Johns Hopkins University School of Medicine, 720 Rutland Ave., Baltimore, MD 21205, USA. Rtuder@JHMI.EDU
Zaiman
Ari L
AL
D000818:Animals; D000959:Antihypertensive Agents / Q000737:chemistry / Q000494:pharmacology / Q000627:therapeutic use; D002455:Cell Division / Q000187:drug effects; D011464:Epoprostenol / Q000031:analogs & derivatives* / Q000737:chemistry / Q000494:pharmacology / Q000502:physiology*; D006801:Humans; D006976:Hypertension, Pulmonary / Q000188:drug therapy / Q000209:etiology / Q000473:pathology / Q000503:physiopathology*; D008168:Lung / Q000378:metabolism / Q000473:pathology; D008954:Models, Biological; D009131:Muscle, Smooth, Vascular / Q000166:cytology / Q000187:drug effects* / Q000378:metabolism; D011651:Pulmonary Artery / Q000166:cytology / Q000187:drug effects* / Q000378:metabolism; D044006:Receptors, Epoprostenol; D011982:Receptors, Prostaglandin / Q000378:metabolism; D015398:Signal Transduction / Q000502:physiology
D000959:Antihypertensive Agents; D044006:Receptors, Epoprostenol; D011982:Receptors, Prostaglandin; D011464:Epoprostenol