Accordingly, we hypothesized that lung senescence lung is associated with a progressive loss of lung fibroblast Thy-1 expression, and that these fibroblasts induce the production of a “pro-fibrotic” matrix that promotes fibrocyte trafficking and retention in response to injury where they undergo myofibroblast transdifferentiation and contribute to subsequent lung fibrosis. This evidence concerns the gene THY1 and pulmonary fibrosis.