Document Detail


New mechanisms of pulmonary arterial hypertension: role of Ca²⁺ signaling.
MedLine Citation:
PMID:  22245772     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Pulmonary arterial hypertension (PAH) is a severe and progressive disease that usually culminates in right heart failure and death if left untreated. Although there have been substantial improvements in our understanding and significant advances in the management of this disease, there is a grim prognosis for patients in the advanced stages of PAH. A major cause of PAH is increased pulmonary vascular resistance, which results from sustained vasoconstriction, excessive pulmonary vascular remodeling, in situ thrombosis, and increased pulmonary vascular stiffness. In addition to other signal transduction pathways, Ca(2+) signaling in pulmonary artery smooth muscle cells (PASMCs) plays a central role in the development and progression of PAH because of its involvement in both vasoconstriction, through its pivotal effect of PASMC contraction, and vascular remodeling, through its stimulatory effect on PASMC proliferation. Altered expression, function, and regulation of ion channels and transporters in PASMCs contribute to an increased cytosolic Ca(2+) concentration and enhanced Ca(2+) signaling in patients with PAH. This review will focus on the potential pathogenic role of Ca(2+) mobilization, regulation, and signaling in the development and progression of PAH.
Authors:
Frank K Kuhr; Kimberly A Smith; Michael Y Song; Irena Levitan; Jason X-J Yuan
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Review     Date:  2012-01-13
Journal Detail:
Title:  American journal of physiology. Heart and circulatory physiology     Volume:  302     ISSN:  1522-1539     ISO Abbreviation:  Am. J. Physiol. Heart Circ. Physiol.     Publication Date:  2012 Apr 
Date Detail:
Created Date:  2012-04-16     Completed Date:  2012-05-30     Revised Date:  2013-06-26    
Medline Journal Info:
Nlm Unique ID:  100901228     Medline TA:  Am J Physiol Heart Circ Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  H1546-62     Citation Subset:  IM    
Affiliation:
Section of Pulmonary, Critical Care, Sleep, and Allergy, Department of Medicine, University of Illinois at Chicago, Chicago, Illinois 60612, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Apoptosis / physiology
Calcium / physiology
Calcium Channels / physiology
Calcium Signaling / physiology*
Carrier Proteins / biosynthesis,  genetics
Caveolae / physiology
Caveolins / biosynthesis
Cell Proliferation
Homeodomain Proteins / biosynthesis,  genetics
Humans
Hypertension, Pulmonary / pathology,  physiopathology*
Myocytes, Smooth Muscle / metabolism,  physiology
Potassium Channels / physiology
Suppressor of Cytokine Signaling Proteins / biosynthesis,  genetics
Transient Receptor Potential Channels / biosynthesis
Vasoconstriction
Grant Support
ID/Acronym/Agency:
P01-HL-098050/HL/NHLBI NIH HHS; P01-HL-098053/HL/NHLBI NIH HHS; R01-HL-066012/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Calcium Channels; 0/Carrier Proteins; 0/Caveolins; 0/Homeodomain Proteins; 0/Potassium Channels; 0/RBX1 protein, human; 0/Suppressor of Cytokine Signaling Proteins; 0/TLX2 protein, human; 0/Transient Receptor Potential Channels; 7440-70-2/Calcium
Comments/Corrections

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


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