Publication: Crosstalk between endothelial cell and thrombus in chronic thromboembolic pulmonary hypertension: perspective
Authors
Sakao, Seiichiro ; Tatsumi, Koichiro
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Publisher
F. Hernández y Juan F. Madrid. Universidad de Murcia: Departamento de Biología Celular e Histología
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DOI
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info:eu-repo/semantics/article
Description
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.
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