Abstract

Radiation-induced pulmonary injury (RIPI) is a common adverse reaction when ionizing radiation acts on the lung. Type II alveolar epithelial cells participate in the process of RIPI by regulating inflammation, epithelial-mesenchymal transition, cellular senescence, etc. The expression of miR-139-5p is inhibited by ionizing radiation, which plays a role in modulating radiotherapy resistance in breast cancer tissues. PIEZO1, a mechano-sensitive ion channel, has been found to play an essential role in bleomycin-induced lung fibrosis. Moreover, there exist some common mechanisms between bleomycin-induced lung fibrosis and RIPI. The stretch changes during RIPI might also regulate PIEZO1 signaling. Furthermore, PIEZO1 is predicted to be a downstream target gene of miR-139-5p, and ionizing radiation leads to increased PIEZO1 mRNA and protein expression. We hypothesized that miR-139-5p might regulate PIEZO1 expression to modulate radiation-induced injury in type II alveolar epithelial cells. Therefore, it is of great practical significance to explore new ways to prevent and treat RIPI and break through the existing research bottlenecks for improving the prevention and treatment of RIPI.

Full Text
Paper version not known

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call