Publication: Role of endothelial-mesenchymal transition in idiopathic portal hypertension
Authors
Sato, Yasunori ; Nakanuma, Yasuni
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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
Idiopathic portal hypertension (IPH) is a
condition of non-cirrhotic portal hypertension without a
known cause of liver disease. Obliterative portal
venopathy is regarded as the primary lesion, which is
responsible for the pre-sinusoidal block of hepatic blood
flow leading to the development of IPH. The disease
pathogenesis of IPH seems to be heterogeneous, and the
pathogenic mechanisms of obliterative portal venopathy
have not been fully understood. Owing to the limited
understanding of the disease pathogenesis, the treatment
of IPH is still largely supportive. Recently, endothelial
dysfunction has been documented during the
development of portal hypertension, and its contribution
to IPH is being analyzed. Endothelial-mesenchymal
transition (EndMT) is a phenomenon whereby vascular
endothelial cells acquire myofibroblastic features
characterized by an ability to express mesenchymal cell
products that are related to tissue fibrogenesis. In
addition to cardiovascular development, there is
increasing evidence showing that EndMT is likely to be
involved in a variety of fibrotic diseases, such as cardiac,
pulmonary, and renal fibrosis. This article reviews the
recent progress in studies of the pathogenic mechanisms
of IPH in terms of endothelial dysfunction of portal
veins. In particular, the role of EndMT in obliterative
portal venopathy of IPH is highlighted and discussed.
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Citation
Histology and Histopathology, vol. 28, nº 2, (2013)
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