Please use this identifier to cite or link to this item:

Title: Crosstalk between endothelial cell and thrombus in chronic thromboembolic pulmonary hypertension: perspective
Issue Date: 2013
Publisher: F. Hernández y Juan F. Madrid. Universidad de Murcia: Departamento de Biología Celular e Histología
Citation: Histology and histopathology, vol. 28, nº 2, (2013)
ISSN: 1699-5848
Related subjects: CDU::6 - Ciencias aplicadas::61 - Medicina
Keywords: Endothelial cell
Abstract: 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 thromboembolism, 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.
Primary author: Sakao, Seiichiro
Tatsumi, Koichiro
Document type: info:eu-repo/semantics/article
Number of pages / Extensions: 9
Rights: info:eu-repo/semantics/openAccess
Appears in Collections:Vol.28, nº 2 (2013)

Files in This Item:
File Description SizeFormat 
Sakao-28-185-193-2013.pdf2,69 MBAdobe PDFView/Open

This item is licensed under a Creative Commons License Creative Commons