MiR-625-5p is a potential therapeutic target in sepsis by regulating CXCL16/CXCR6 axis and endothelial barrier.

Background: MicroRNA plays an important role in the progression of sepsis. We found a significant increase of in miR-625-5p expression in the blood of patients with sepsis, and lipopolysaccharide (LPS)-stimulated EA.hy926 cells.

NETs induce ferroptosis of endothelial cells in LPS-ALI through SDC-1/HS and downstream pathways.

Background: Extracellular neutrophil extracellular traps (NETs) play an important role in acute lung injury (ALI), but their mechanisms are still unclear. The aim of this study is to explore the effects of NETs on endothelial glycocalyx/HGF/cMET pathway and ferroptosis in ALI and elucidate their potential mechanisms.

Methods: Plasma was collected from healthy and sepsis patients to test for differences in neutrophil elastase (NE) expression of NETs components.

PLD2 deletion alleviates disruption of tight junctions in sepsis-induced ALI by regulating PA/STAT3 phosphorylation pathway.

Background: Increased inflammatory exudation caused by endothelium and endothelial junction damage is a typical pathological feature of acute respiratory distress syndrome/acute lung injury (ARDS/ALI). Previous studies have shown that phospholipase D2 (PLD2) can increase the inflammatory response and has a close relationship with the severity of sepsis-induced ALI and the mortality of sepsis, but its mechanism is unknown. This study explored the effect and mechanism of PLD2 deletion on the structure and function of endothelial tight junction (TJ) in lipopolysaccharide (LPS)-induced ALI.