摘要
Dear Editor,COVID-19,SARS,and MERS are featured by suppressed lungfibrinolysis.The primary objective of this study was to decipherthe role of the fibrinolytic niche in the progenitor alveolar type 2(AT2)cell-mediated re-alveolarization.The expression of Piau inAT2 cells has been confirmed at the mRNA,protein,and functionallevel across species.We employed influenza-infected&Plau^(-/-)mice,3D organoids,and polarized monolayers to track AT2 fate.We found a marked reduction in total AT2 cells and CD44^(+)subpopulation when the fibrinolytic niche was disrupted.
基金
supported by NIH grant R01 HL134828.