Regulatory role of ncRNAs in pulmonary epithelial and endothelial barriers: Molecular therapy clues of influenza-induced acute lung injury

Influenza A virus is globally widespread, causing a large number of infections and deaths due to acute lung injury (ALI) every year. The destruction and impairment of alveolar epithelial and microvascular endothelial cell barrier functions are the key inducers of ALI and acute respiratory distress syndrome caused by influenza virus infection. Although noncoding ribonucleic acids (ncRNAs) do not encode proteins in host cells, they possess the ability of protein regulation and signal transduction. Moreover, studies have shown that ncRNAs are significantly and differentially expressed following influenza virus infection, and these ncRNAs play vital roles in the pathogenesis of influenza virus infection. By analyzing the recently published literature, we found that ncRNA could regulate alveolar epithelial and microvascular endothelial cell barrier functions in different ways, which include influencing the innate and acquired immune responses of host cells, affecting apoptosis and autophagy, regulating tight and adherent junctions, etc. In the present paper, we reviewed the roles and regulatory mechanisms of these ncRNAs and discussed the effects of these ncRNAs on pulmonary epithelial and endothelial cell barriers. Further, by sorting and analyzing available research data, we proposed the possibility of applying these ncRNAs for treating ALI in influenza cases, thereby alleviating the permeability of pulmonary epithelial and endothelial cell barriers. Moreover, we discussed future research and development prospects. Our review suggests that targeted therapy and drug research based on ncRNAs would provide an important direction for the molecular therapy of influenza-induced ALI.