The DOI matches its Crossref record; 61 of the 61 references it cites were found in a registry or an index.
Hypoxia-inducible factors: Crosstalk between inflammation and metabolism
Abstract
Hypoxia-inducible factors (HIFs) are oxygen-sensitive transcription factors that allow adaptation to hypoxic environments. HIFs function in the cellular response to stress: metabolic, hypoxic, or inflammatory. Metabolic changes occur during tumorigenesis that are, in part, under hypoxia and HIF regulation. Additionally, inflammatory signaling and infiltration secondary to hypoxia are clear drivers of tumor progression. HIF-1α and HIF-2α have opposing and occasionally overlapping roles in both tumor cells and inflammatory cells within the tumor microenvironment and crosstalk between these populations has clear effects on tumor metabolism, inflammation, and progression. It is becoming increasingly apparent that HIFs are one common link between hypoxia, chronic inflammation, metabolic adaptation, and tumor progression through its function in macrophages during cancer development.
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“TNF, PGE2, and TLR activation have been linked to chronic granulomatous inflammation such as in tuberculosis or granulomatous listeriosis”
From Transcriptome-Based Network Analysis Reveals a Spectrum Model of Human Macrophage Activation (2014) · cites this paper as Shay and Celeste Simon, 2012
In the citing paper
“For macrophages stimulated with TPP, the TF network also included STAT4 , as well as TFs associated with negative regulation of TLR signaling ( HEY1 ; Hu et al., 2008), macrophage activation ( TGIF1 ; Ramsey et al., 2008), or TFs at the interface between inflammation and metabolism ( HIF1A ; Shay and Celeste Simon, 2012).”
From Transcriptome-Based Network Analysis Reveals a Spectrum Model of Human Macrophage Activation (2014) · cites this paper as Shay and Celeste Simon, 2012
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Metadata
- Authors
- Shay, J. E. S., & Celeste Simon, M.
- Venue
- Seminars in Cell & Developmental Biology
- Publisher
- Elsevier BV
- Published
- 2012-06
- Volume
- 23
- Issue
- 4
- Pages
- 389-394
- ISSN
- 1084-9521
- Cited by
- 122
- References
- 61
- Language
- en
- Licence
- www.elsevier.com/tdm/userlicense/1.0/ (tdm)
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