Our study suggests that miR-27a-3p selectively blocked the TGF-β1/Smad pathways to suppress the myofibroblast differentiation and targeted the TRL4/IRAK4 pathway to restrain DCs maturation, thus attenuating BOS. Our findings suggest that miR-27a-3p is a potential active molecule on BOS management after lung transplantation.
Keyphrases
- transforming growth factor
- dendritic cells
- epithelial mesenchymal transition
- high glucose
- diabetic rats
- immune response
- extracorporeal membrane oxygenation
- inflammatory response
- toll like receptor
- drug induced
- endothelial cells
- signaling pathway
- cancer therapy
- oxidative stress
- risk assessment
- mouse model
- pulmonary fibrosis
- regulatory t cells
- nuclear factor
- drug delivery