Sirt1 deletion leads to enhanced inflammation and aggravates endotoxin-induced acute kidney injury. Academic Article uri icon

abstract

  • Bacterial endotoxin has been known to induce excessive inflammatory responses and acute kidney injury. In the present study, we used a mouse model of endotoxemia to investigate the role of Sirt1 in inflammatory kidney injury. We examined molecular and cellular responses in inducible Sirt1 knockout (Sirt1-/-) mice and wild type littermates (Sirt1+/+) in lipopolysaccharide (LPS)-induced kidney injury. Our studies demonstrated that Sirt1 deletion caused aggravated kidney injury, which was associated with increased inflammatory responses including elevated pro-inflammatory cytokine production, and increased ICAM-1 and VCAM-1 expression. Inflammatory signaling such as STAT3/ERK phosphorylation and NF-B activation was markedly elevated in kidney tissues of Sirt1 knockout mice after LPS challenge. The results indicate that Sirt1 is protective against LPS-induced acute kidney injury by suppressing kidney inflammation and down-regulating inflammatory signaling.

published proceedings

  • PLoS One

altmetric score

  • 0.25

author list (cited authors)

  • Gao, R., Chen, J., Hu, Y., Li, Z., Wang, S., Shetty, S., & Fu, J.

citation count

  • 67

complete list of authors

  • Gao, Rong||Chen, Jiao||Hu, Yuxin||Li, Zhenyu||Wang, Shuxia||Shetty, Sreerama||Fu, Jian

editor list (cited editors)

  • Wu, M.

publication date

  • January 2014