Hypoxia promotes fibrogenesis in vivo via HIF-1 stimulation of epithelial-to-mesenchymal transition.

By D. Higgins, K. Kimura, W. Bernhardt, N. Shrimanker, Y. Akai, B. Hohenstein, Yoshihiko Saito, Richard J. Johnson, M. Kretzler, C. Cohen and 3 more. Journal of Clinical Investigation, 2007

982 citations recorded by the source corpus.

Subfields: Cancer Research, Genetics

View Paper: https://www.semanticscholar.org/paper/661c4d0604f6f47711ff8f20fb94f8ff281b34c8

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Cancer Research

1. M. Sofroniew
2. J. López-Novoa
3. M. Nieto
4. E. Lengyel
5. N. Ferrara
6. Marcus E. Peter
7. Rakesh K. Jain
8. Jing Yang

In Genetics

1. M. Nieto
2. J. López-Novoa
3. E. Lengyel
4. R. Weinberg

Citations in the corpus

• Inflammation and EMT: an alliance towards organ fibrosis and cancer progression (2009, background): “…also enhances Snail1 activity by activating the expression of its partners lysyl-oxidases (LOX) both in the kidney after UUO and in cancer cells, thereby promoting fibrogenesis and tumour progression through the reinforcement of the EMT programme (Higgins et al, 2007; Sahlgren et al, 2008) (Fig 3).”
• The miR-200 family determines the epithelial phenotype of cancer cells by targeting the E-cadherin repressors ZEB1 and ZEB2. (2008, background): “Interestingly, for both ZEB genes, mRNA degradation was suggested to be the mechanism of suppression rather than translational silencing (Hurteau et al. 2006; Christoffersen et al. 2007).”
• Fibroblasts and myofibroblasts in wound healing (2014, neutral): “In some cells at least, there is cross talk between hypoxia signaling and TGF-β signaling that may exacerbate matrix synthesis and thus fibrosis.(63,64)”
• Antiangiogenic therapy elicits malignant progression of tumors to increased local invasion and distant metastasis. (2009, neutral): “systems (Higgins et al., 2007; Munoz-Najar et al., 2006; Pennacchietti et al., 2003).”
• Astrocyte-derived VEGF-A drives blood-brain barrier disruption in CNS inflammatory disease. (2012, background): “To inactivate Hif1a selectively in vivo, we crossed mGfapCre mice with a floxed Hif1a allele (37).”
• Oxidant Mechanisms in Renal Injury and Disease (2016, positive): “Moderately increased mitochondria ROS results in stabilization of hypoxia-inducible factor (HIF) in endothelial cells (99) and in stimulating nuclear factor-E2-related factor (NRF-2) (235), effects that are both protective against oxidative stress and renoprotective (107,196).”
• Hypoxia-Inducible Factor 1α Induces Fibrosis and Insulin Resistance in White Adipose Tissue (2009, background): “As such, another interesting candidate could be CTGF, which has been shown to be regulated in a fashion similar to that of LOX in the adipocyte (46).”