期刊
INTERNATIONAL IMMUNOPHARMACOLOGY
卷 125, 期 -, 页码 -出版社
ELSEVIER
DOI: 10.1016/j.intimp.2023.111074
关键词
Sepsis-induced myocardial dysfunction; Lipopolysaccharide; Polo -like kinase 1; NF-xB
In sepsis, Plk-1 promotes the development of SIMD. Inhibition of Plk-1 improves LPS-induced myocardial injury and inflammation, and enhances the survival rate of mice. Plk-1 inhibition also impedes NF-κB signal pathway activation.
Sepsis-induced myocardial dysfunction (SIMD) is the main cause of mortality in sepsis. In this study, we identified Polo-like kinase 1 (Plk-1) is a promoter of SIMD. Plk-1 expression was increased in lipopolysaccharide (LPS)-treated mouse hearts and neonatal rat cardiomyocytes (NRCMs). Inhibition of Plk-1 either by heterozygous deletion of Plk-1 or Plk-1 inhibitor BI 6727 alleviated LPS-induced myocardial injury, inflammation, cardiac dysfunction, and thereby improved the survival of LPS-treated mice. Plk-1 was identified as a kinase of inhibitor of kappa B kinase alpha (IKK alpha). Plk-1 inhibition impeded NF-xB signal pathway activation in LPS-treated mouse hearts and NRCMs. Augmented Plk-1 is thus essential for the development of SIMD and is a druggable target for SIMD.
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