Hypoxia and hypoxia inducible factors: Diverse roles in liver diseases

Hypoxia has been shown to have a role in the pathogenesis of several forms of liver disease. The hypoxia inducible factors (HIFs) are a family of evolutionarily conserved transcriptional regulators that affect a homeostatic response to low oxygen tension and have been identified as key mediators of...

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Published in:Hepatology (Baltimore, Md.) Vol. 55; no. 2; pp. 622 - 633
Main Authors: Nath, Bharath, Szabo, Gyongyi
Format: Journal Article
Language:English
Published: Hoboken Wiley Subscription Services, Inc., A Wiley Company 01-02-2012
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Abstract Hypoxia has been shown to have a role in the pathogenesis of several forms of liver disease. The hypoxia inducible factors (HIFs) are a family of evolutionarily conserved transcriptional regulators that affect a homeostatic response to low oxygen tension and have been identified as key mediators of angiogenesis, inflammation, and metabolism. In this review we summarize the evidence for a role of HIFs across a range of hepatic pathophysiology. We describe regulation of the HIFs and review investigations that demonstrate a role for HIFs in the development of liver fibrosis, activation of innate immune pathways, hepatocellular carcinoma, as well as other liver diseases in both human disease as well as murine models. (HEPATOLOGY 2012;)
AbstractList Hypoxia has been shown to have a role in the pathogenesis of several forms of liver disease. The hypoxia inducible factors (HIFs) are a family of evolutionarily conserved transcriptional regulators that affect a homeostatic response to low oxygen tension and have been identified as key mediators of angiogenesis, inflammation, and metabolism. In this review we summarize the evidence for a role of HIFs across a range of hepatic pathophysiology. We describe regulation of the HIFs and review investigations that demonstrate a role for HIFs in the development of liver fibrosis, activation of innate immune pathways, hepatocellular carcinoma, as well as other liver diseases in both human disease as well as murine models. (HEPATOLOGY 2012; )
Hypoxia has been shown to have a role in the pathogenesis of several forms of liver disease. The hypoxia inducible factors (HIFs) are a family of evolutionarily conserved transcriptional regulators that affect a homeostatic response to low oxygen tension and have been identified as key mediators of angiogenesis, inflammation, and metabolism. In this review we summarize the evidence for a role of HIFs across a range of hepatic pathophysiology. We describe regulation of the HIFs and review investigations that demonstrate a role for HIFs in the development of liver fibrosis, activation of innate immune pathways, hepatocellular carcinoma, as well as other liver diseases in both human disease as well as murine models.
Hypoxia has been shown to have a role in the pathogenesis of several forms of liver disease. The Hypoxia Inducible Factors (HIFs) are a family of evolutionarily conserved transcriptional regulators that affect a homeostatic response to low oxygen tension and have been identified as key mediators of angiogenesis, inflammation, and metabolism. In this review, we summarize the evidence for a role of HIFs across a range of hepatic pathophysiology. We describe regulation of the hypoxia inducible factors and review investigations that demonstrate a role for HIFs in the development of liver fibrosis, activation of innate immune pathways, hepatocellular carcinoma, as well as other liver diseases in both human disease as well as murine models.
Author Szabo, Gyongyi
Nath, Bharath
Author_xml – sequence: 1
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  fullname: Nath, Bharath
  organization: Department of Medicine, University of Massachusetts Medical School, Worcester, MA
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  givenname: Gyongyi
  surname: Szabo
  fullname: Szabo, Gyongyi
  email: gyongyi.szabo@umassmed.edu
  organization: Department of Medicine, University of Massachusetts Medical School, Worcester, MA
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Issue 2
Keywords Digestive diseases
Hypoxia
Hepatic disease
Oxygen
Gastroenterology
Language English
License CC BY 4.0
Copyright © 2011 American Association for the Study of Liver Diseases.
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Potential conflict of interest: Dr. Szabo is a consultant for, advises, and is on the speakers' bureau of Vertex, Conatus, GlaxoSmithKline, Bristol-Myers Squibb, Idenix, Idera, Integrated Therapeutics, Johnson & Johnson, Novartis, Novelos, Ocera, Roche, Schering-Plough, Wyeth, SmithKline Beechman, Ikaria, and FALK.
ArticleID:HEP25497
Potential conflict of interest: Dr. Szabo is a consultant for, advises, and is on the speakers' bureau of Vertex, Conatus, GlaxoSmithKline, Bristol‐Myers Squibb, Idenix, Idera, Integrated Therapeutics, Johnson & Johnson, Novartis, Novelos, Ocera, Roche, Schering‐Plough, Wyeth, SmithKline Beechman, Ikaria, and FALK.
fax: 508‐856‐4770
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OpenAccessLink https://onlinelibrary.wiley.com/doi/pdfdirect/10.1002/hep.25497
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PublicationTitle Hepatology (Baltimore, Md.)
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Snippet Hypoxia has been shown to have a role in the pathogenesis of several forms of liver disease. The hypoxia inducible factors (HIFs) are a family of...
Hypoxia has been shown to have a role in the pathogenesis of several forms of liver disease. The Hypoxia Inducible Factors (HIFs) are a family of...
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SubjectTerms Acetaminophen - poisoning
Animals
Biological and medical sciences
Gastroenterology. Liver. Pancreas. Abdomen
Hepatology
Humans
Hypoxia
Hypoxia - complications
Hypoxia - metabolism
Hypoxia-Inducible Factor 1 - metabolism
Immunity, Innate
Lipid Metabolism
Liver - drug effects
Liver - metabolism
Liver cirrhosis
Liver diseases
Liver Diseases - etiology
Liver Diseases - metabolism
Liver Regeneration
Liver. Biliary tract. Portal circulation. Exocrine pancreas
Medical sciences
Metals - metabolism
Oxygen - metabolism
Reperfusion Injury - metabolism
Sleep Apnea, Obstructive - metabolism
Title Hypoxia and hypoxia inducible factors: Diverse roles in liver diseases
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https://onlinelibrary.wiley.com/doi/abs/10.1002%2Fhep.25497
https://www.ncbi.nlm.nih.gov/pubmed/22120903
https://www.proquest.com/docview/1766825557
https://search.proquest.com/docview/1776646538
https://pubmed.ncbi.nlm.nih.gov/PMC3417333
Volume 55
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