
DOI . ORG {
}
Title[redir]:
Hypoxia-Inducible Factors as Essential Regulators of Inflammation | SpringerLink
Description:
Myeloid cells provide important functions in low oxygen (O2) environments created by pathophysiological conditions, including sites of infection, inflammation, tissue injury, and solid tumors. Hypoxia-inducible factors (HIFs) are principle regulators of hypoxic...
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Keywords {π}
google, scholar, pubmed, cas, article, hypoxia, macrophages, cancer, hypoxiainducible, factor, tumor, expression, hifalpha, cell, inflammation, immunol, human, med, lee, simon, cells, lewis, chapter, biol, res, harris, progression, hypoxic, role, activation, macrophage, function, factors, gene, angiogenesis, hif, interleukin, alpha, kim, celeste, tumors, hifs, regulation, therapy, necrosis, factoralpha, johnson, usa, arthritis, privacy,
Topics {βοΈ}
nuclear factor-kappab-dependent pathway von hippel-lindau protein-independent hif-1alpha-dependent nf-kappab activity pi3k-hif-1alpha-vegf axis hypoxia-inducible factors hif-1alpha hypoxia-inducible factor-1Ξ± regulation hypoxia-inducible factor-2 alpha month download article/chapter hypoxia-inducible factor induction hif-dependent signalling events hypoxia-inducible factor 1alpha hypoxia inducible factor-1alpha hypoxia-inducible factor-1alpha desferrioxamine-stimulated hmc-1 cells hypoxia-induced neutrophil survival carboxyl-terminal transactivation activity tumor necrosis factor-alpha hif-1Ξ± promotes survival myd88-dependent il-6 production bone marrow-derived macrophages leukocyte-endothelial adhesion molecules lipopolysaccharide-induced sepsis cytokine-driven compensatory proliferation hif-1alpha expression regulates hypoxia-inducible factor hypoxia-inducible factor 1 myeloid cell-mediated inflammation tumour necrosis factor hypoxia-inducible factors hypoxia-inducible factors 1 o2-regulated prolyl hydroxylation hif-1-dependent induction nf-kappab activation privacy choices/manage cookies macrophage inflammatory protein-2 myeloid cell function tumor necrosis factor device instant download septic shock syndrome anti-cancer therapy important transcriptional effectors editor information editors adjuvant-induced arthritis chapter diverse effects il-10 increases lethality dendritic cells liver parenchymal cells deliver gene therapy hif-1 transcriptional activity myeloid cell inflammation
Questions {β}
- Balkwill F, Mantovani A (2001) Inflammation and cancer: back to Virchow?
Schema {πΊοΈ}
ScholarlyArticle:
headline:Hypoxia-Inducible Factors as Essential Regulators of Inflammation
pageEnd:120
pageStart:105
image:https://media.springernature.com/w153/springer-static/cover/book/978-3-642-13329-9.jpg
genre:
Biomedical and Life Sciences
Biomedical and Life Sciences (R0)
isPartOf:
name:Diverse Effects of Hypoxia on Tumor Progression
isbn:
978-3-642-13329-9
978-3-642-13328-2
type:Book
publisher:
name:Springer Berlin Heidelberg
logo:
url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
type:ImageObject
type:Organization
author:
name:Hongxia Z. Imtiyaz
affiliation:
name:University of Pennsylvania
address:
name:Abramson Family Cancer Research Institute, University of Pennsylvania, Philadelphia, USA
type:PostalAddress
type:Organization
name:Howard Hughes Medical Institute
address:
name:Howard Hughes Medical Institute, Chevy Chase, USA
type:PostalAddress
type:Organization
type:Person
name:M. Celeste Simon
affiliation:
name:University of Pennsylvania
address:
name:Abramson Family Cancer Research Institute, University of Pennsylvania, Philadelphia, USA
type:PostalAddress
type:Organization
name:Howard Hughes Medical Institute
address:
name:Howard Hughes Medical Institute, Chevy Chase, USA
type:PostalAddress
type:Organization
name:University of Pennsylvania School of Medicine
address:
name:Department of Cell and Developmental Biology, University of Pennsylvania School of Medicine, Philadelphia, USA
type:PostalAddress
type:Organization
email:[email protected]
type:Person
keywords:Rheumatoid Arthritis Pathogenesis, Aryl Hydrocarbon Receptor Nuclear Translocator, Rheumatoid Arthritis Joint, Macrophage Gene Expression, Endothelial Monocyte Activate Polypeptide
description:Myeloid cells provide important functions in low oxygen (O2) environments created by pathophysiological conditions, including sites of infection, inflammation, tissue injury, and solid tumors. Hypoxia-inducible factors (HIFs) are principle regulators of hypoxic adaptation, regulating gene expression involved in glycolysis, erythropoiesis, angiogenesis, proliferation, and stem cell function under low O2. Interestingly, increasing evidence accumulated over recent years suggests an additional important regulatory role for HIFs in inflammation. In macrophages, HIFs not only regulate glycolytic energy generation, but also optimize innate immunity, control pro-inflammatory gene expression, mediate bacterial killing and influence cell migration. In neutrophils, HIF-1Ξ± promotes survival under O2-deprived conditions and mediates blood vessel extravasation by modulating Ξ²
2 integrin expression. Additionally, HIFs contribute to inflammatory functions in various other components of innate immunity, such as dendritic cells, mast cells, and epithelial cells. This review will dissect the role of each HIF isoform in myeloid cell function and discuss their impact on acute and chronic inflammatory disorders. Currently, intensive studies are being conducted to illustrate the connection between inflammation and tumorigenesis. Detailed investigation revealing interaction between microenvironmental factors such as hypoxia and immune cells is needed. We will also discuss how hypoxia and HIFs control properties of tumor-associated macrophages and their relationship to tumor formation and progression.
datePublished:2010
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name:University of Pennsylvania
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name:Hongxia Z. Imtiyaz
affiliation:
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address:
name:Abramson Family Cancer Research Institute, University of Pennsylvania, Philadelphia, USA
type:PostalAddress
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name:Howard Hughes Medical Institute
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name:Howard Hughes Medical Institute, Chevy Chase, USA
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name:M. Celeste Simon
affiliation:
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address:
name:Abramson Family Cancer Research Institute, University of Pennsylvania, Philadelphia, USA
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email:[email protected]
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name:Abramson Family Cancer Research Institute, University of Pennsylvania, Philadelphia, USA
name:Howard Hughes Medical Institute, Chevy Chase, USA
name:Abramson Family Cancer Research Institute, University of Pennsylvania, Philadelphia, USA
name:Howard Hughes Medical Institute, Chevy Chase, USA
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