In summary, we have demonstrated that p53 and its transcriptional target miR-34a regulate glycolysis in lung fibroblasts, and CSP7, when used as a therapeutic agent, ramps down the elevated key enzymes involved in glycolytic pathways in multiple preclinical mouse models of established pulmonary fibrosis and in isolated hfLfs and mfLfs via restoration of p53 and miR-34a expression. Here, TP53 is linked to pulmonary fibrosis.