Document Detail

Crosstalk between endothelial cell and thrombus in chronic thromboembolic pulmonary hypertension: perspective.
MedLine Citation:
PMID:  23275302     Owner:  NLM     Status:  In-Data-Review    
It is generally accepted that chronic thromboembolic pulmonary hypertension (CTEPH) results from pulmonary emboli originating from deep vein thrombosis. However, this consensus opinion has been challenged, and the concept that some aspects of CTEPH exacerbation might result from a small-vessel disease leading to secondary thrombosis has been suggested. In addition to the effect of recurrent thrombo-embolism, a number of lines of clinical evidence indicate that progressive worsening is contributed to by remodeling in the small pulmonary arteries. Histopathological studies of the microvascular changes in CTEPH have identified vascular lesions similar to those seen in idiopathic pulmonary arterial hypertension (IPAH). Especially in in vitro and ex vivo experiments, pulmonary artery endothelial cells (ECs) in pulmonary hypertensive diseases are suggested to exhibit an unusual hyperproliferative potential with decreased susceptibility to apoptosis, indicating that dysfunctional ECs may contribute to the progression of the diseases. Although the degree and mechanisms of EC dysfunction as a contributor to CTEPH are unclear, EC dysfunction may occur in small arteries. Indeed, the cells stimulated by the microenvironment created by the unresolved clot may release substances that induce EC dysfunction. The EC dysfunctions in CTEPH may lead to disorders of the anti-coagulation properties in ECs and may result in additional clots in situ. Moreover, these may lead to the progression, not only of distal thrombus, but also of proximal clotting. This article reviews the pathobiological concepts of CTEPH and explains a crosstalk between EC dysfunction and in situ thrombi which may contribute to the vascular lesions of CTEPH.
S Sakao; K Tatsumi
Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  Histology and histopathology     Volume:  28     ISSN:  1699-5848     ISO Abbreviation:  Histol. Histopathol.     Publication Date:  2013 Feb 
Date Detail:
Created Date:  2012-12-31     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  8609357     Medline TA:  Histol Histopathol     Country:  Spain    
Other Details:
Languages:  eng     Pagination:  185-93     Citation Subset:  IM    
Department of Respirology (B2), Graduate School of Medicine, Chiba University, Chuo-ku, Chiba, Japan.
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