Therefore, the objectives of the present study were: (1) to determine whether HIF-1α and CHOP proteins were co-expressed by AECs in lung tissue from IPF patients; (2) to evaluate whether micro-environmental hypoxia could activate the UPR pathways in rat AECs; (3) to decipher the molecular mechanisms linking hypoxia, HIF-1α, ER stress and apoptosis in these cells. This evidence concerns the gene HIF1A and idiopathic pulmonary fibrosis.