ACTA1 and pulmonary fibrosis: In vitro cultured AECs can undergo epithelial-mesenchymal transition (EMT) through the activation of Notch and other signaling pathways and become a partial source of myofibroblasts (MFBs); MFBs can express the specific biomarker α-SMA; this protein is involved in contraction and migration and the excessively secreted extracellular matrix (ECM), which causes the deposition and accumulation of ECM and ultimately leads to the progression of pulmonary fibrosis [41].