Similarly, the increased expression of miR-326 attenuated pulmonary fibrosis in mice exposed to silica, and the relevant mechanism might be that miR-326 inhibited inflammation and promoted autophagy activity through the target protein tumor necrosis factor superfamily 14 (TNFSF14) and polypyrimidine tract-binding protein 1 (PTBP1), respectively [59]. Here, PTBP1 is linked to pulmonary fibrosis.