In summary, we provide a new mechanistic insight into lung fibrosis and determine that megakaryocytes migrate to the BLM-injured lung through the CXCL12/CXCR4 axis and megakaryocytes promote the proliferation and trans-differentiation of fibroblasts partially through direct contact or TGF-β1 pathway (Fig. 7). Here, TGFB1 is linked to pulmonary fibrosis.