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Article Abstract
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.
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| http://dx.doi.org/10.1016/j.intimp.2025.115477 | DOI Listing |
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