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Effects of hypoxia and hyperoxia on the differential expression of VEGF-A isoforms and receptors in Idiopathic Pulmonary Fibrosis (IPF)

Research output: Contribution to journalLetter

Original languageEnglish
Article number9
Number of pages5
JournalRespiratory Research
DateAccepted/In press - 26 Dec 2017
DatePublished (current) - 15 Jan 2018


Dysregulation of VEGF-A bioavailability has been implicated in the development of lung injury/fibrosis, exemplified by Idiopathic Pulmonary Fibrosis (IPF). VEGF-A is a target of the hypoxic response via its translational regulation by HIF-1α. The role of hypoxia and hyperoxia in the development and progression of IPF has not been explored. In normal lung (NF) and IPF-derived fibroblasts (FF) VEGF-Axxxa protein expression was upregulated by hypoxia, mediated through activation of VEGF-Axxxa gene transcription. VEGF-A receptors and co-receptors were differentially expressed by hypoxia and hyperoxia. Our data supports a potential role for hypoxia, hyperoxia and VEGF-Axxxa isoforms as drivers of fibrogenesis.

    Research areas

  • Hypoxia, Idiopathic pulmonary fibrosis, Interstitial lung disease, Vascular endothelial growth factor

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    Licence: CC BY


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