The crowded crossroad to angiogenesis in systemic sclerosis: where is the key to the problem?

In systemic sclerosis (SSc), peripheral vasculopathy is characterized by a progressive and irreversible loss of capillaries following endothelial cell injury, due to defects in both vascular repair and expected increase in new vessel growth (angiogenesis). The discovery of key molecular targets may...

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Detalles Bibliográficos
Autores principales: Manetti, Mirko, Guiducci, Serena, Matucci-Cerinic, Marco
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2016
Materias:
Editorial
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4743122/
https://www.ncbi.nlm.nih.gov/pubmed/26847365
http://dx.doi.org/10.1186/s13075-016-0937-x
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author Manetti, Mirko
Guiducci, Serena
Matucci-Cerinic, Marco
author_facet Manetti, Mirko
Guiducci, Serena
Matucci-Cerinic, Marco
author_sort Manetti, Mirko
collection PubMed
description In systemic sclerosis (SSc), peripheral vasculopathy is characterized by a progressive and irreversible loss of capillaries following endothelial cell injury, due to defects in both vascular repair and expected increase in new vessel growth (angiogenesis). The discovery of key molecular targets may help to develop the most effective therapeutic strategy for the SSc-related vasculopathy. A pathway worth targeting in SSc may include vascular endothelial growth factor, 165b isoform, an endogenous angiogenesis inhibitor abnormally expressed and released by different cell types, including activated endothelial cells and platelets.
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spelling pubmed-47431222016-02-06 The crowded crossroad to angiogenesis in systemic sclerosis: where is the key to the problem? Manetti, Mirko Guiducci, Serena Matucci-Cerinic, Marco Arthritis Res Ther Editorial In systemic sclerosis (SSc), peripheral vasculopathy is characterized by a progressive and irreversible loss of capillaries following endothelial cell injury, due to defects in both vascular repair and expected increase in new vessel growth (angiogenesis). The discovery of key molecular targets may help to develop the most effective therapeutic strategy for the SSc-related vasculopathy. A pathway worth targeting in SSc may include vascular endothelial growth factor, 165b isoform, an endogenous angiogenesis inhibitor abnormally expressed and released by different cell types, including activated endothelial cells and platelets. BioMed Central 2016-02-05 2016 /pmc/articles/PMC4743122/ /pubmed/26847365 http://dx.doi.org/10.1186/s13075-016-0937-x Text en © Manetti et al. 2016 Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
spellingShingle Editorial
Manetti, Mirko
Guiducci, Serena
Matucci-Cerinic, Marco
The crowded crossroad to angiogenesis in systemic sclerosis: where is the key to the problem?
title The crowded crossroad to angiogenesis in systemic sclerosis: where is the key to the problem?
title_full The crowded crossroad to angiogenesis in systemic sclerosis: where is the key to the problem?
title_fullStr The crowded crossroad to angiogenesis in systemic sclerosis: where is the key to the problem?
title_full_unstemmed The crowded crossroad to angiogenesis in systemic sclerosis: where is the key to the problem?
title_short The crowded crossroad to angiogenesis in systemic sclerosis: where is the key to the problem?
title_sort crowded crossroad to angiogenesis in systemic sclerosis: where is the key to the problem?
topic Editorial
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4743122/
https://www.ncbi.nlm.nih.gov/pubmed/26847365
http://dx.doi.org/10.1186/s13075-016-0937-x
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