Emerging therapies for pulmonary arterial hypertension.
Pulmonary arterial hypertension is characterised by increased pulmonary vascular resistance due to increased vascular tone and structural remodelling of pulmonary vessels. The therapies that are in use so far have been developed to correct endothelial dysfunction and reduce vasomotor tone. These treatments have a limited effect on the remodelling process and, increasingly, the focus is turning to potent strategies for inhibiting vascular proliferation and promoting vascular apoptosis. Multiple novel targets have been uncovered over the last 5 years and several are now in early clinical trials. At present, it is clear that there is no single treatment for the condition. Although this is the case, studies are investigating the role of combining therapies that are already established.
Ali
Omar
O
Imperial College London, Experimental Medicine & Toxicology, Hammersmith Hospital, London, UK.
Wharton
John
J
Gibbs
John Simon Russell
JS
Howard
Luke
L
Wilkins
Martin Russell
MR
D015106:3',5'-Cyclic-GMP Phosphodiesterases / Q000037:antagonists & inhibitors; D000818:Animals; D002121:Calcium Channel Blockers / Q000627:therapeutic use; D000242:Cyclic AMP / Q000378:metabolism; D006152:Cyclic GMP / Q000378:metabolism; D054706:Cyclic Nucleotide Phosphodiesterases, Type 5; D065130:Endothelin A Receptor Antagonists; D006801:Humans; D006976:Hypertension, Pulmonary / Q000188:drug therapy* / Q000235:genetics / Q000503:physiopathology; D010597:Pharmacogenetics; D044062:Prostaglandins I / Q000627:therapeutic use; D011651:Pulmonary Artery
D002121:Calcium Channel Blockers; D065130:Endothelin A Receptor Antagonists; D044062:Prostaglandins I; D000242:Cyclic AMP; D015106:3',5'-Cyclic-GMP Phosphodiesterases; D054706:Cyclic Nucleotide Phosphodiesterases, Type 5; C517381:PDE5A protein, human; D006152:Cyclic GMP