Document Detail


Molecular pathogenesis of pulmonary arterial hypertension.
MedLine Citation:
PMID:  18596905     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Recent investigations have suggested that it might be possible to reverse the pathology of pulmonary arterial hypertension (PAH), a disorder that can be rapidly progressive and fatal despite current treatments including i.v. prostacyclin. This review will address the cellular and molecular processes implicated in clinical, genetic, and experimental studies as underlying the pulmonary vascular abnormalities associated with PAH. Emerging treatments are aimed at inducing apoptosis of abnormal vascular cells that obstruct blood flow and at promoting regeneration of "lost" distal vasculature.
Authors:
Marlene Rabinovitch
Related Documents :
16969145 - Hyperthyroidism: a rare cause of reversible pulmonary hypertension.
16581695 - Pulmonary arterial hypertension.
17573495 - Is pulmonary arterial hypertension in neurofibromatosis type 1 secondary to a plexogeni...
17268125 - Bosentan improved syncope in a hemodialysis patient with pulmonary hypertension and mil...
3478085 - An investigation of possible age-related changes in the inferior alveolar artery in man.
1155805 - The systemic arterial pattern of the guinea pig: the abdomen.
Publication Detail:
Type:  Journal Article; Review    
Journal Detail:
Title:  The Journal of clinical investigation     Volume:  118     ISSN:  0021-9738     ISO Abbreviation:  J. Clin. Invest.     Publication Date:  2008 Jul 
Date Detail:
Created Date:  2008-07-03     Completed Date:  2008-09-25     Revised Date:  2014-09-19    
Medline Journal Info:
Nlm Unique ID:  7802877     Medline TA:  J Clin Invest     Country:  United States    
Other Details:
Languages:  eng     Pagination:  2372-9     Citation Subset:  AIM; IM    
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:
Animals
Bone Morphogenetic Protein Receptors, Type II / physiology
Humans
Hypertension, Pulmonary / etiology,  physiopathology*,  therapy
Inflammation Mediators / physiology
Ion Channels / physiology
Leukocyte Elastase / metabolism
Mesenchymal Stromal Cells / physiology
Models, Biological*
Vasodilator Agents / therapeutic use
Grant Support
ID/Acronym/Agency:
R01 HL087118/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Inflammation Mediators; 0/Ion Channels; 0/Vasodilator Agents; EC 2.7.11.30/Bone Morphogenetic Protein Receptors, Type II; EC 3.4.21.37/Leukocyte Elastase
Comments/Corrections

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


Previous Document:  Rituximab administration in third trimester of pregnancy suppresses neonatal B-cell development.
Next Document:  A role for polyploidy in the tumorigenicity of Pim-1-expressing human prostate and mammary epithelia...