HIF-1alpha is essential for myeloid cell-mediated inflammation.
By T. Cramer, Y. Yamanishi, B. Clausen, I. Förster, R. Pawlinski, N. Mackman, V. Haase, R. Jaenisch, M. Corr, V. Nizet and 4 more. Cell, 2003
1,025 citations recorded by the source corpus.
Subfields: Cancer Research, Genetics, Immunology
View Paper: https://www.semanticscholar.org/paper/b80d827c1d55b73be84ea9f6a4f89c5e360ca244
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In Cancer Research
- M. C. Simon
- Craig B. Thompson
- Ralph J. Deberardinis
- Guido Kroemer
- B. Keith
- G. Semenza
- V. Nizet
- Cheng-Jun Hu
In Genetics
- P. Martín-Sanz
- Juan-Carlos Rodríguez-Prados
- M. C. Simon
- Guido Kroemer
- Mihai G. Netea
- Daniel Rico
- B. Keith
- P. Murray
In Immunology
- Guido Kroemer
- A. Chawla
- Luke A. O'Neill
- P. Murray
- C. Lewis
- K. Ganeshan
- Craig B. Thompson
- Mihai G. Netea
Citations in the corpus
- Differential Roles of Hypoxia-Inducible Factor 1α (HIF-1α) and HIF-2α in Hypoxic Gene Regulation (2003, positive): “This finding is consistent with previous data indicating that HIF-1 is necessary for glycolytic capacity in multiple cells, such as granulocytes, monocytes/ macrophages (20), chondrocytes (86), and MEFs (91).”
- The biology of cancer: metabolic reprogramming fuels cell growth and proliferation. (2008, background): “HIF-1 activity requires the subunit HIF-1 a ,whichisexpressedunderthecontrolofgrowth-factorsig-naling, in particular the PI3K/Akt/mTOR pathway (Cramer et al., 2003; Jiang et al., 2001; Majumder et al., 2004).”
- HIF Transcription Factors, Inflammation, and Immunity (2014, background): “Notably, myeloid HIF-1a contributes to inflammation in rheumatoid arthritis synovial tissue (Cramer et al., 2003), which is hypoxic (Konisti et al., 2012).”
- Substrate Fate in Activated Macrophages: A Comparison between Innate, Classic, and Alternative Activation (2010, positive): “Mice with myeloid lineage-specific HIF1a floxed-UBC-cre/ERT(2) mice for conditional HIF1a inactivation were used (24, 25) and were a generous gift of M.”
- Hypoxia-induced angiogenesis: good and evil. (2011, background): “HIF-1α may also play a role in TAM-mediated angiogenesis, as HIF-1α regulates the glycolytic phenotype of TAMs and promotes migration, invasion, and aggregation of TAMs at sites of inflammation.(92) Indeed, HIF signaling regulates tumor vascular growth not only by regulating genes in tumor cells and”
- mTOR- and HIF-1α–mediated aerobic glycolysis as metabolic basis for trained immunity (2014, background): “can be observed in myeloid cell-specific HIF1α conditional knock-out mice (mHIF1α-KO) (27).”
- Molecular Mechanisms That Influence the Macrophage M1–M2 Polarization Balance (2014, background): “Although HIF-1α and HIF-2α displayed physiologically antagonistic functions, their antiphase regulation allows them to coordinately regulate NO production to guide macrophage polarization.”
- Tumor cell metabolism: cancer's Achilles' heel. (2008, background): “Within TAMs, HIF-1 is essential to upregulate glycolysis so that the cells can migrate into tumor beds (Cramer et al., 2003).”
- Adipocyte-derived Th2 cytokines and myeloid PPARdelta regulate macrophage polarization and insulin sensitivity. (2008, background): “On the other hand, glycolysis is known to provide the energy required to mount an inflammatory response (Cramer et al., 2003; Kim et al., 2006; Seagroves et al., 2001).”
- Mechanisms regulating the recruitment of macrophages into hypoxic areas of tumors and other ischemic tissues. (2004, background): “is crucial for macrophage accumulation in inflammatory sites such as the hypoxic synovia or arthritic joints in mice.(95) It would be interesting to see whether ET-1 or ET-2 up-regulates HIF-1α expression by monocytes or macrophages respectively in the”
- Oxidative metabolism and PGC-1beta attenuate macrophage-mediated inflammation. (2006, background): “Recent studies have shown a key role for glycolytic pathways controlled by hypoxia inducible factor-1α (HIF-1α) in promoting the effector responses of classically activated macrophages (Cramer et al., 2003).”