Abstract
During idiopathic pulmonary fibrosis (IPF) exacerbations, alveolar hypoxia can occur as well as in chronic forms with tissue remodeling and in patients with obstructive sleep apnea hypopnea syndrome (OSAH).In rat alveolar epithelial cells, hypoxia induces apoptosis and mesenchymal stem cell (MSC) conditioned medium reduces this process.Hypoxia induces 2 signaling pathways: HIF and reactive oxygen species (ROS) pathways. It also induces proapoptotic factors such as Bnip 3 or CHOP. MSC can block these pathways through a paracrine effect involving the release of keratinocyte growth factor (KGF).In vitro, hypoxia also enhances epithelial to mesenchymal transition (EMT) of alveolar cells through the production of profibrotic mediators such as TGF β. MSC prevent the emergence of harmful effects via the release of KGF.There is a strong association between OSAH and incident IPF. Chronic intermittent hypoxia (CIH) associated with OSAH can induce oxydative stress and the pro-inflammatory NFκB pathway. CIH exacerbates animal mortality, lung inflammation and fibrosis in vivo in mice treated with bleomycin.
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