| First Author | Gao Z | Year | 2023 |
| Journal | Int Immunopharmacol | Volume | 125 |
| Issue | Pt A | Pages | 111074 |
| PubMed ID | 37879229 | Mgi Jnum | J:342377 |
| Mgi Id | MGI:7548150 | Doi | 10.1016/j.intimp.2023.111074 |
| Citation | Gao Z, et al. (2023) Polo-like kinase 1 promotes sepsis-induced myocardial dysfunction. Int Immunopharmacol 125(Pt A):111074 |
| abstractText | 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 (IKKalpha). Plk-1 inhibition impeded NF-kappaB 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. |
