Lung microvascular endothelial inflammation and barrier dysfunction play critical roles in the pathogenesis of acute lung injury (ALI)/acute respiratory distress syndrome (ARDS). Despite recent scientific advances, the mortality of ALI/ARDS is still extremely high because the molecular mechanisms involved in ALI/ARDS remain unclear. In a recent issue of the journal Advanced Science, Baoyinna and colleagues reported that deubiquitinase USP30 induces lung microvascular inflammation and endothelial barrier disruption through the S-adenosylmethionine (SAM) cycle, DNA methylation, and miR-30a-5p down-regulation in ALI/ARDS. Their findings provide a strong rationale for targeting microRNAs, S-adenosylmethionine, DNA methylation, and deubiquitinating enzymes as potential therapeutic strategies for the treatment of ALI/ARDS.
Su Yunchao (Thu,) studied this question.