Document Detail


Molecular mechanisms of pulmonary hypertension.
MedLine Citation:
PMID:  19361468     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The pathogenesis of pulmonary arterial hypertension (PAH) is complex, involving multiple modulating genes and environmental factors. Multifactorial impairment of the physiologic balance can lead to vasoconstriction, vascular smooth muscle cell and endothelial cell proliferation/fibrosis, inflammation, remodeling and in-situ thrombosis. These are the likely mechanisms that lead to narrowing of the vessel followed by progressive increase in pulmonary vascular resistance and the clinical manifestations of pulmonary hypertension. Subsequently, major goal of the therapy is to avoid acute pulmonary vasoconstriction, halt the progression of vascular remodeling, and reverse the early vascular remodeling if possible. Recently published data addressing certain molecular mechanisms for pathogenesis of PAH have led to the successful therapeutic interventions. This review will focus on the common and critical molecular pathways including genetic basis of the development of PAH that on the whole may be new targets for therapeutic interventions.
Authors:
Pinar Yildiz
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Publication Detail:
Type:  Journal Article; Review     Date:  2009-01-31
Journal Detail:
Title:  Clinica chimica acta; international journal of clinical chemistry     Volume:  403     ISSN:  1873-3492     ISO Abbreviation:  Clin. Chim. Acta     Publication Date:  2009 May 
Date Detail:
Created Date:  2009-04-27     Completed Date:  2009-07-06     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  1302422     Medline TA:  Clin Chim Acta     Country:  Netherlands    
Other Details:
Languages:  eng     Pagination:  9-16     Citation Subset:  IM    
Affiliation:
Department of Pulmonology, Yedikule Chest Disease and Surgery Training and Research Hospital, Zeytinburnu Istanbul, Turkey. pinary70@yahoo.com
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MeSH Terms
Descriptor/Qualifier:
Animals
Genomics
Humans
Hypertension, Pulmonary / enzymology,  genetics,  metabolism*,  pathology
Proteomics

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