VNN1 aggravates sepsis by promoting inflammation and oxidative stress through PPARγ signaling VNN1 in sepsis.

Vanin-1 (VNN1) is crucial in inflammatory response and oxidative stress (OS), yet its contribution to sepsis remains unidentified. In this study, we investigated the functions of VNN1 in sepsis. Our results indicated VNN1 was elevated in sepsis patients and positively correlated with various cytokines. Meanwhile, VNN1 elevated in a mouse model of sepsis. In VNN1 knockout (KO) mice, VNN1 deficiency improved survival and organ function following CLP-induced sepsis. Furthermore, sepsis-induced inflammation and OS were reduced in VNN1 KO mice. Furthermore, our findings indicated VNN1 deficiency alleviated sepsis by regulating NF-kB/PPARγ pathways. Finally, the results showed VNN1 increased in sepsis patients, and higher VNN1 were associated with a poorer prognosis of sepsis. Our findings revealed a novel molecular mechanism in which VNN1 participated in sepsis by regulating NF-kB/PPARγ. This study offered a new strategy for inhibiting sepsis by targeting VNN1 signaling pathways.