As a doctoral candidate, I have gotten a hybrid training on computational skills and biological skills. My research contributions focused on epithelial cell reprogramming in lung aging and lung fibrosis. More specifically, I phenotyped the lung epithelial cells and identified cellular senescence as a common type of reprogramming in both alveolar and airway regions during lung aging and lung fibrosis. I compared the cell population in young and old mice and demonstrated declined population of epithelial cells (EpCAM+) in old mice. Further analysis demonstrated increased activity of β-catenin and senescence-associated β-galactosidase (SA-β-GAL) in primary AT2 cells in aging mice. Similarly, I compared epithelial cell subpopulation in lung tissue from IPF patients and health donors and revealed an enlarged population of airway epithelial cells and sharply declined population of AT2 cells in IPF patients. I further identified G-protein coupled receptor 87 (GPR87) as a novel marker of airway basal cells within honeycombs cysts in IPF. Then I investigated the role of developmental pathway within both alveolar and airway regions and demonstrated the activation of developmental signaling pathway contributing to epithelial cell senescence. My work highlighted the significance and connection of developmental signaling pathway and cellular senescence during the development of IPF. Furthermore, I generated two datasets of single cell RNA-sequencing, with one from lung tissue of young healthy donors and old healthy donors, the other one from lung tissue of health donors and IPF patients. Both datasets were enriched with EpCAM+ cells isolated from parenchymal lung tissue, providing high-resolution of epithelial cell atlas to the research community of lung aging and lung fibrosis.