CTRP3 mitigates sepsis-induced impairment of endothelial barrier function by suppressing pyroptosis in endothelial cells.

Acute lung injury significantly contributes to mortality in bacterial sepsis due to lung endothelial barrier destruction, leading to protein-rich lung edema, an influx of proinflammatory leukocytes, and persistent hypoxemia. CTRP3, an adipokine, reduces endothelial adhesion molecules Vcam-1 and Icam-1 and inhibits LPS-induced monocytic adhesion, highlighting its anti-inflammatory effects. This study investigates CTRP3's protective role in sepsis-induced acute lung injury, revealing reduced CTRP3 expression during sepsis, which worsens endothelial dysfunction. Supplementing with recombinant CTRP3 mitigates this dysfunction and reduces LPS-induced endothelial pyroptosis by inhibiting caspase-1, thus protecting the endothelial barrier and reducing lung injury. In conclusion, CTRP3 preserves endothelial function in sepsis by suppressing pyroptosis.