Silencing of Prdx3 abolished the beneficial effects of YAP1, indicating the vital role of the YAP1/TEAD1-Prdx3 axis in inhibiting cellular senescence and maintaining cell survival, whereas overexpression of Prdx3 in AT2 cells alleviated pulmonary fibrosis. This evidence concerns the gene PRDX3 and pulmonary fibrosis.