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Antiangiogenic therapy for portal hypertension in liver cirrhosis: Current progress and perspectives

Developing medicines for hemodynamic disorders that are characteristic of cirrhosis of the liver is a relevant problem in modern hepatology. The increase in hepatic vascular resistance to portal blood flow and subsequent hyperdynamic circulation underlie portal hypertension (PH) and promote its prog...

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Autores principales: Garbuzenko, Dmitry Victorovich, Arefyev, Nikolay Olegovich, Kazachkov, Evgeniy Leonidovich
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Baishideng Publishing Group Inc 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6127663/
https://www.ncbi.nlm.nih.gov/pubmed/30197479
http://dx.doi.org/10.3748/wjg.v24.i33.3738
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author Garbuzenko, Dmitry Victorovich
Arefyev, Nikolay Olegovich
Kazachkov, Evgeniy Leonidovich
author_facet Garbuzenko, Dmitry Victorovich
Arefyev, Nikolay Olegovich
Kazachkov, Evgeniy Leonidovich
author_sort Garbuzenko, Dmitry Victorovich
collection PubMed
description Developing medicines for hemodynamic disorders that are characteristic of cirrhosis of the liver is a relevant problem in modern hepatology. The increase in hepatic vascular resistance to portal blood flow and subsequent hyperdynamic circulation underlie portal hypertension (PH) and promote its progression, despite the formation of portosystemic collaterals. Angiogenesis and vascular bed restructurization play an important role in PH pathogenesis as well. In this regard, strategic directions in the therapy for PH in cirrhosis include selectively decreasing hepatic vascular resistance while preserving or increasing portal blood flow, and correcting hyperdynamic circulation and pathological angiogenesis. The aim of this review is to describe the mechanisms of angiogenesis in PH and the methods of antiangiogenic therapy. The PubMed database, the Google Scholar retrieval system, and the reference lists from related articles were used to search for relevant publications. Articles corresponding to the aim of the review were selected for 2000-2017 using the keywords: “liver cirrhosis”, “portal hypertension”, “pathogenesis”, “angiogenesis”, and “antiangiogenic therapy”. Antiangiogenic therapy for PH was the inclusion criterion. In this review, we have described angiogenesis inhibitors and their mechanism of action in relation to PH. Although most of them were studied only in animal experiments, this selective therapy for abnormally growing newly formed vessels is pathogenetically reasonable to treat PH and associated complications.
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spelling pubmed-61276632018-09-07 Antiangiogenic therapy for portal hypertension in liver cirrhosis: Current progress and perspectives Garbuzenko, Dmitry Victorovich Arefyev, Nikolay Olegovich Kazachkov, Evgeniy Leonidovich World J Gastroenterol Minireviews Developing medicines for hemodynamic disorders that are characteristic of cirrhosis of the liver is a relevant problem in modern hepatology. The increase in hepatic vascular resistance to portal blood flow and subsequent hyperdynamic circulation underlie portal hypertension (PH) and promote its progression, despite the formation of portosystemic collaterals. Angiogenesis and vascular bed restructurization play an important role in PH pathogenesis as well. In this regard, strategic directions in the therapy for PH in cirrhosis include selectively decreasing hepatic vascular resistance while preserving or increasing portal blood flow, and correcting hyperdynamic circulation and pathological angiogenesis. The aim of this review is to describe the mechanisms of angiogenesis in PH and the methods of antiangiogenic therapy. The PubMed database, the Google Scholar retrieval system, and the reference lists from related articles were used to search for relevant publications. Articles corresponding to the aim of the review were selected for 2000-2017 using the keywords: “liver cirrhosis”, “portal hypertension”, “pathogenesis”, “angiogenesis”, and “antiangiogenic therapy”. Antiangiogenic therapy for PH was the inclusion criterion. In this review, we have described angiogenesis inhibitors and their mechanism of action in relation to PH. Although most of them were studied only in animal experiments, this selective therapy for abnormally growing newly formed vessels is pathogenetically reasonable to treat PH and associated complications. Baishideng Publishing Group Inc 2018-09-07 2018-09-07 /pmc/articles/PMC6127663/ /pubmed/30197479 http://dx.doi.org/10.3748/wjg.v24.i33.3738 Text en ©The Author(s) 2018. Published by Baishideng Publishing Group Inc. All rights reserved. http://creativecommons.org/licenses/by-nc/4.0/ This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial.
spellingShingle Minireviews
Garbuzenko, Dmitry Victorovich
Arefyev, Nikolay Olegovich
Kazachkov, Evgeniy Leonidovich
Antiangiogenic therapy for portal hypertension in liver cirrhosis: Current progress and perspectives
title Antiangiogenic therapy for portal hypertension in liver cirrhosis: Current progress and perspectives
title_full Antiangiogenic therapy for portal hypertension in liver cirrhosis: Current progress and perspectives
title_fullStr Antiangiogenic therapy for portal hypertension in liver cirrhosis: Current progress and perspectives
title_full_unstemmed Antiangiogenic therapy for portal hypertension in liver cirrhosis: Current progress and perspectives
title_short Antiangiogenic therapy for portal hypertension in liver cirrhosis: Current progress and perspectives
title_sort antiangiogenic therapy for portal hypertension in liver cirrhosis: current progress and perspectives
topic Minireviews
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6127663/
https://www.ncbi.nlm.nih.gov/pubmed/30197479
http://dx.doi.org/10.3748/wjg.v24.i33.3738
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