Sirt1 deletion leads to enhanced inflammation and aggravates endotoxin-induced acute kidney injury.
Sirt1 deletion leads to enhanced inflammation and aggravates endotoxin-induced acute kidney injury.
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DOI：
10.1371/journal.pone.0098909
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发表时间：
2014
期刊：
影响因子：
3.7
通讯作者：
Fu J
中科院分区：
文献类型：
--
作者：
Gao R;Chen J;Hu Y;Li Z;Wang S;Shetty S;Fu J
已知细菌内毒素可诱导过度炎症反应和急性肾损伤。在本研究中，我们使用内毒素血症小鼠模型来研究Sirt 1在炎症性肾损伤中的作用。我们研究了诱导型Sirt 1敲除（Sirt 1 −/−）小鼠和野生型同窝小鼠（Sirt 1 +/+）在脂多糖（LPS）诱导的肾损伤中的分子和细胞反应。我们的研究表明，Sirt 1缺失导致肾损伤加重，这与炎症反应增加有关，包括促炎细胞因子产生增加，ICAM-1和VCAM-1表达增加。Sirt 1基因敲除小鼠肾组织中炎症信号如STAT 3/ERK磷酸化和NF-κB活化在LPS攻击后显著升高。结果表明，Sirt 1通过抑制肾脏炎症和下调炎症信号而对LPS诱导的急性肾损伤具有保护作用。
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-κB 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.
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影响因子：
3.9
作者：
Hwang, Jae-woong;Chung, Sangwoon;Sundar, Isaac K.;Yao, Hongwei;Arunachalam, Gnanapragasam;McBurney, Michael W.;Rahman, Irfan
通讯作者：
Rahman, Irfan
DOI：
10.1186/bcr1632
发表时间：
2007
期刊：
Breast cancer research : BCR
影响因子：
--
作者：
Li H;Rajendran GK;Liu N;Ware C;Rubin BP;Gu Y
通讯作者：
Gu Y
影响因子：
64.5
作者：
Chang HC;Guarente L
通讯作者：
Guarente L
影响因子：
4.4
作者：
Greenhill, Claire J.;Rose-John, Stefan;Jenkins, Brendan J.
通讯作者：
Jenkins, Brendan J.
脂多糖诱导的HSF1敲除小鼠的严重多器官损伤与中性粒细胞浸润和粘附分子表面表达的增加有关
影响因子：
5.5
作者：
Chen, Shuhua;Zuo, Xiaoxia;Xiao, Xianzhong
通讯作者：
Xiao, Xianzhong