Ferroptotic stress promotes endothelial dysfunction in sepsis-induced lung injury (IMAGE)

Sichuan International Medical Exchange and Promotion Association

Ferroptotic stress promotes endothelial dysfunction in sepsis-induced lung injury

Caption

Our study, for the first time, discovered the regulatory effects of glycolysis-derived H3K14la on ferroptosis in sepsis-induced lung injury and revealed that H3K14la activated ECs by modulating the gene transcription of TFRC and SLC40A1. The inhibition of lactate production decreased H3K14la levels, which suppressed EC ferroptosis and thereby reduced EC activation, alleviating sepsis-induced lung injury

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Dr. Ying Chen

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