Pulmonary arterial hypertension: a look to the future.

The Third World Symposium on Pulmonary Arterial Hypertension served not only as a forum for the presentation of state-of-the art overviews of the pathobiologic and clinical aspects of pulmonary arterial hypertension (PAH), but also afforded an opportunity to the international scientific community to explore future directions of research and collaboration. This summary provides a brief overview of future directions in the field.

[1]  M. Gladwin,et al.  Right ventricular function and failure: report of a National Heart, Lung, and Blood Institute working group on cellular and molecular mechanisms of right heart failure. , 2006, Circulation.

[2]  S. Said Mediators and modulators of pulmonary arterial hypertension. , 2006, American journal of physiology. Lung cellular and molecular physiology.

[3]  W. Seeger,et al.  Reversal of experimental pulmonary hypertension by PDGF inhibition. , 2005, The Journal of clinical investigation.

[4]  R. Barst,et al.  A RANDOMIZED, DOUBLE-BLIND, PLACEBO-CONTROLLED STUDY OF ILOPROST INHALATION AS ADD-ON THERAPY TO BOSENTAN IN PULMONARY ARTERIAL HYPERTENSION (PAH) , 2005 .

[5]  W. Seeger,et al.  Imatinib for the treatment of pulmonary arterial hypertension. , 2005, The New England journal of medicine.

[6]  D. Stewart,et al.  Rescue of Monocrotaline-Induced Pulmonary Arterial Hypertension Using Bone Marrow–Derived Endothelial-Like Progenitor Cells: Efficacy of Combined Cell and eNOS Gene Therapy in Established Disease , 2005, Circulation research.

[7]  J. Yuan,et al.  Pathogenesis of pulmonary arterial hypertension: the need for multiple hits. , 2005, Circulation.

[8]  K. Kangawa,et al.  Adrenomedullin in the treatment of pulmonary hypertension , 2004, Peptides.

[9]  J. Dötsch,et al.  Brief adrenomedullin inhalation leads to sustained reduction of pulmonary artery pressure , 2004, European Respiratory Journal.

[10]  K. Kaibuchi,et al.  Long-Term Treatment With a Rho-Kinase Inhibitor Improves Monocrotaline-Induced Fatal Pulmonary Hypertension in Rats , 2004, Circulation research.

[11]  G. Berry,et al.  Simvastatin Rescues Rats From Fatal Pulmonary Hypertension by Inducing Apoptosis of Neointimal Smooth Muscle Cells , 2003, Circulation.

[12]  G. Funk,et al.  Vasoactive intestinal peptide as a new drug for treatment of primary pulmonary hypertension. , 2003, The Journal of clinical investigation.

[13]  P. Thistlethwaite,et al.  Signaling molecules in nonfamilial pulmonary hypertension. , 2003, The New England journal of medicine.

[14]  G. Berry,et al.  Simvastatin attenuates smooth muscle neointimal proliferation and pulmonary hypertension in rats. , 2002, American journal of respiratory and critical care medicine.

[15]  J. Yuan,et al.  Ion channels in pulmonary arterial hypertension. , 2002, Progress in cardiovascular diseases.

[16]  W. Seeger,et al.  Inhaled iloprost for severe pulmonary hypertension. , 2002, The New England journal of medicine.

[17]  M. Humbert,et al.  Effects of beraprost sodium, an oral prostacyclin analogue, in patients with pulmonary arterial hypertension: a randomized, double-blind, placebo-controlled trial. , 2002, Journal of the American College of Cardiology.

[18]  Avid,et al.  BOSENTAN THERAPY FOR PULMONARY ARTERIAL HYPERTENSION , 2002 .

[19]  M. Humbert,et al.  Serotonin transporter overexpression is responsible for pulmonary artery smooth muscle hyperplasia in primary pulmonary hypertension. , 2001, The Journal of clinical investigation.

[20]  L. Rubin,et al.  Augmented K(+) currents and mitochondrial membrane depolarization in pulmonary artery myocyte apoptosis. , 2001, American journal of physiology. Lung cellular and molecular physiology.

[21]  K. Kangawa,et al.  Haemodynamic and hormonal effects of adrenomedullin in patients with pulmonary hypertension , 2000, Heart.

[22]  M. Humbert,et al.  Sporadic primary pulmonary hypertension is associated with germline mutations of the gene encoding BMPR-II, a receptor member of the TGF-β family , 2000, Journal of medical genetics.

[23]  S. Hodge,et al.  Familial primary pulmonary hypertension (gene PPH1) is caused by mutations in the bone morphogenetic protein receptor-II gene. , 2000, American journal of human genetics.

[24]  R. Trembath,et al.  Heterozygous germline mutations in BMPR2, encoding a TGF-β receptor, cause familial primary pulmonary hypertension , 2000, Nature Genetics.

[25]  C. Indolfi,et al.  Effects of hydroxymethylglutaryl coenzyme A reductase inhibitor simvastatin on smooth muscle cell proliferation in vitro and neointimal formation in vivo after vascular injury. , 2000, Journal of the American College of Cardiology.

[26]  D. Badesch,et al.  Prostacyclin synthase expression is decreased in lungs from patients with severe pulmonary hypertension. , 1999, American journal of respiratory and critical care medicine.

[27]  J. Orens,et al.  Dysfunctional voltage-gated K+ channels in pulmonary artery smooth muscle cells of patients with primary pulmonary hypertension. , 1998, Circulation.

[28]  B. Fanburg,et al.  A new role for an old molecule: serotonin as a mitogen. , 1997, The American journal of physiology.

[29]  B. Groves,et al.  A comparison of continuous intravenous epoprostenol (prostacyclin) with conventional therapy for primary pulmonary hypertension. , 1996, The New England journal of medicine.

[30]  B. Groves,et al.  An imbalance between the excretion of thromboxane and prostacyclin metabolites in pulmonary hypertension. , 1992, The New England journal of medicine.