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Targeting Hypoxia Inducible Factors-1α As a Novel Therapy in Fibrosis

Fibrosis, characterized by increased extracellular matrix (ECM) deposition, and widespread vasculopathy, has the prominent trait of chronic hypoxia. Hypoxia inducible factors-1α (HIF-1α), a key transcriptional factor in response to this chronic hypoxia, is involved in fibrotic disease, such as Syste...

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Detalles Bibliográficos
Autores principales: Xiong, Anji, Liu, Yi
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5447768/
https://www.ncbi.nlm.nih.gov/pubmed/28611671
http://dx.doi.org/10.3389/fphar.2017.00326
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author Xiong, Anji
Liu, Yi
author_facet Xiong, Anji
Liu, Yi
author_sort Xiong, Anji
collection PubMed
description Fibrosis, characterized by increased extracellular matrix (ECM) deposition, and widespread vasculopathy, has the prominent trait of chronic hypoxia. Hypoxia inducible factors-1α (HIF-1α), a key transcriptional factor in response to this chronic hypoxia, is involved in fibrotic disease, such as Systemic sclerosis (SSc). The implicated function of HIF-1α in fibrosis include stimulation of excessive ECM, vascular remodeling, and futile angiogenesis with further exacerbation of chronic hypoxia and deteriorate pathofibrogenesis. This review will focus on the molecular biological behavior of HIF-1α in regulating progressive fibrosis. Better understanding of the role for HIF-1α-regulated pathways in fibrotic disease will accelerate development of novel therapeutic strategies that target HIF-1α. Such new therapeutic strategies may be particularly effective for treatment of the prototypic, multisystem fibrotic, autoimmune disease SSc.
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spelling pubmed-54477682017-06-13 Targeting Hypoxia Inducible Factors-1α As a Novel Therapy in Fibrosis Xiong, Anji Liu, Yi Front Pharmacol Pharmacology Fibrosis, characterized by increased extracellular matrix (ECM) deposition, and widespread vasculopathy, has the prominent trait of chronic hypoxia. Hypoxia inducible factors-1α (HIF-1α), a key transcriptional factor in response to this chronic hypoxia, is involved in fibrotic disease, such as Systemic sclerosis (SSc). The implicated function of HIF-1α in fibrosis include stimulation of excessive ECM, vascular remodeling, and futile angiogenesis with further exacerbation of chronic hypoxia and deteriorate pathofibrogenesis. This review will focus on the molecular biological behavior of HIF-1α in regulating progressive fibrosis. Better understanding of the role for HIF-1α-regulated pathways in fibrotic disease will accelerate development of novel therapeutic strategies that target HIF-1α. Such new therapeutic strategies may be particularly effective for treatment of the prototypic, multisystem fibrotic, autoimmune disease SSc. Frontiers Media S.A. 2017-05-30 /pmc/articles/PMC5447768/ /pubmed/28611671 http://dx.doi.org/10.3389/fphar.2017.00326 Text en Copyright © 2017 Xiong and Liu. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Pharmacology
Xiong, Anji
Liu, Yi
Targeting Hypoxia Inducible Factors-1α As a Novel Therapy in Fibrosis
title Targeting Hypoxia Inducible Factors-1α As a Novel Therapy in Fibrosis
title_full Targeting Hypoxia Inducible Factors-1α As a Novel Therapy in Fibrosis
title_fullStr Targeting Hypoxia Inducible Factors-1α As a Novel Therapy in Fibrosis
title_full_unstemmed Targeting Hypoxia Inducible Factors-1α As a Novel Therapy in Fibrosis
title_short Targeting Hypoxia Inducible Factors-1α As a Novel Therapy in Fibrosis
title_sort targeting hypoxia inducible factors-1α as a novel therapy in fibrosis
topic Pharmacology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5447768/
https://www.ncbi.nlm.nih.gov/pubmed/28611671
http://dx.doi.org/10.3389/fphar.2017.00326
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