For pulmonary diseases, Willis et al. [47] reported both in vivo and in vitro that UCMSC-EXOs effectively regulate macrophage phenotypes, suppressing proinflammatory M1 states (CCL2, CCL7, and IL-6) while promoting anti-inflammatory M2-like states (arginase-1, CD206, and CCL17), and these findings demonstrate the potential of UCMSC-EXOs to alleviate bronchopulmonary dysplasia induced by hyperoxia by normalizing lung function, reducing fibrosis and pulmonary vascular remodeling, and ameliorating pulmonary hypertension. This evidence concerns the gene CCL17 and fibrosis.