What question did this study set out to answer?

To investigate how NDRG1 contributes to sepsis-induced acute lung injury through specific signaling pathways.

February 13, 2026Open Access

NDRG1 aggravates Sepsis-Induced acute lung injury via PKM2-dependent activation of STAT3 and NF-κB signaling

Key Points

To investigate how NDRG1 contributes to sepsis-induced acute lung injury through specific signaling pathways.
In vitro and in vivo analysis of NDRG1's effects on lung injury related to sepsis.
Assessment of the role of PKM2 in activating downstream STAT3 and NF-κB pathways.
Evaluation of inflammatory responses and endothelial integrity as outcomes of the intervention.
NDRG1 was found to enhance inflammatory responses in lung tissues during sepsis.
Activation of PKM2 was linked to the increased activity of both STAT3 and NF-κB pathways.
Disruption of endothelial integrity was observed, correlating with worse lung injury.

Abstract

By orchestrating downstream STAT3 and NF-κB signaling cascades through PKM2 dependency, NDRG1 contributes to the progression of septic lung injury via increased inflammatory responses and disruption of endothelial integrity. Intervening in this signaling route may offer a viable avenue for therapeutic management of lung injury linked to sepsis.

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NDRG1 aggravates Sepsis-Induced acute lung injury via PKM2-dependent activation of STAT3 and NF-κB signaling

Key Points

Abstract

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