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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Main Authors: Anji Xiong (Author), Yi Liu (Author)
Format: Book
Published: Frontiers Media S.A., 2017-05-01T00:00:00Z.
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042 |a dc 
100 1 0 |a Anji Xiong  |e author 
700 1 0 |a Yi Liu  |e author 
245 0 0 |a Targeting Hypoxia Inducible Factors-1α As a Novel Therapy in Fibrosis 
260 |b Frontiers Media S.A.,   |c 2017-05-01T00:00:00Z. 
500 |a 1663-9812 
500 |a 10.3389/fphar.2017.00326 
520 |a 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. 
546 |a EN 
690 |a fibrosis 
690 |a chronic hypoxia 
690 |a hypoxia inducible factor 
690 |a targeted therapy 
690 |a systemic sclerosis 
690 |a Therapeutics. Pharmacology 
690 |a RM1-950 
655 7 |a article  |2 local 
786 0 |n Frontiers in Pharmacology, Vol 8 (2017) 
787 0 |n http://journal.frontiersin.org/article/10.3389/fphar.2017.00326/full 
787 0 |n https://doaj.org/toc/1663-9812 
856 4 1 |u https://doaj.org/article/cdde40faf7c8486fb4a7e3cc33f7b4df  |z Connect to this object online.