While dysfunctional alveolar epithelial cells type II (AECII) are thought to be central to the initiation of IPF, the mechanisms by which AECIIs provoke fibrosis are uncertain. Independent studies have shown that markers of cellular senescence (p53, p21, and p16INK4A) are upregulated in AECIIs in IPF lungs within the remodeled fibrotic areas. Despite the detection of senescent AECIIs in fibrotic lungs, their role in fibrogenesis is unknown and their secretory phenotype (SASP) remains undefined. In addition, senescent fibroblasts have also been detected in pulmonary fibrotic tissue. Interestingly, unlike many organs where the fibrosis never resolves, dermal fibrosis can undergo spontaneous regression despite the constant detection of senescent fibroblasts. We, therefore, hypothesize that the dynamic changes in the SASP from profibrotic to pro-resolution occurs in skin but not in lungs resulting in fibrosis reversal only in the skin. Using transgenic mouse strains and pharmacological senolytic treatment, we will determine how Sn cells have the potential to regulate fibrogenesis and its resolution by switching their SASP factors expression over time. Our findings will have important implications for how emerging senolytic drugs, which have the potential to provide novel therapeutic benefits for the treatment of SSc, should best be administered.