Figure 1.

Schematic diagram illustration of the role of MSCs and secretion of their EVs in the treatment of hyperoxia-induced lung injury. As the preterm neonatal lung is exposed to excessive oxygen supplementation (hyperoxia) or infection (sepsis), proinflammatory cytokines are released, anti-inflammatory cytokines are inhibited, and oxidative stress occurs. These changes direct the conversion of M2 to M1 macrophage subsets, leading to structural lung damage/developmental abnormalities. MSCs are derived from various sources including bone marrow (BM), umbilical cord (UC), placenta, and adipose tissue. Treatment with MSCs or their secreted EVs alleviates the hyperoxia-induced lung injury through several mechanisms. These mechanisms include inhibition of proinflammatory cytokines and induction of anti-inflammatory cytokines, VEGF, and antioxidant pathways, leading to the transition of M1 to M2 macrophages, and the stimulation of differentiation of AT2 alveolar epithelial cells to AT1 alveolar epithelial cells. This illustration was created using BioRender.com.