TGFB1 and idiopathic pulmonary fibrosis: The exosomes can also be antifibrotic: (i) exosomes from alveolar type II cells control macrophage differentiation, favor mitochondrial biogenesis, and enhance oxidative phosphorylation [146], (ii) exosomes from bronchial epithelial cells inhibit WNT5A and WNT10B, modifying their interaction with TGFβ1 [147], (iii) exosomes in the sera of IPF patients are low in miR-30b, which, via Runx1-Spred2, can reduce fibrosis and inflammation in the murine model [148], (iv) miR-142-3p from macrophage exosomes can be taken by AECs and lung fibroblasts, and reduce TGFβ, TβR1, COL1A1, and COL3A1 [149].