p66Shc signaling does not contribute to tubular damage induced by renal ischemia-reperfusion injury in rat.
p66Shc signaling does not contribute to tubular damage induced by renal ischemia-reperfusion injury in rat.
复制标题
DOI：
10.1016/j.bbrc.2022.03.020
复制
发表时间：
2022-05-07
影响因子：
3.1
通讯作者：
Sorokin A
中科院分区：
文献类型：
--
作者：
Miller B;Regner K;Sorokin A
肾缺血再灌注（IR）损伤是急性肾损伤的主要原因之一，也是肾移植的重要危险因素。肾损伤的程度受缺血持续时间的影响，并且是由过量产生的活性氧（ROS）引起的。已知接头蛋白 p66Shc 可以调节细胞和器官对氧化应激的敏感性，并在应激条件下对线粒体过氧化氢的产生做出显着贡献。在培养的肾细胞中进行的研究表明，p66Shc 介导的线粒体功能障碍和 ROS 产生是肾缺血性损伤的原因。我们使用缺乏 p66Shc 表达或表达 p66Shc 变体的转基因大鼠来评估 p66Shc 信号传导对缺血再灌注大鼠模型中肾损伤的潜在贡献。对外髓小管损伤的分析表明，在大鼠模型中，p66Shc 表达或其组成型信号传导对 IR 损伤没有贡献。
Renal ischemia-reperfusion (IR) injury is one of the major causes of acute kidney injury and represents a significant risk factor for renal transplantation. The level of renal damage is influenced by the ischemic duration and is caused by excessive amounts of produced reactive oxygen species (ROS). Adaptor protein p66Shc is known to regulate cellular and organ’s sensitivity to oxidative stress and to contribute significantly to mitochondrial production of hydrogen peroxide in stress conditions. Studies carried out in cultured renal cells suggest that p66Shc-mediated mitochondrial dysfunction and ROS production are responsible for renal ischemic injury. We used our genetically modified rats, which either lack p66Shc expression, or express p66Shc variant, which constitutively generates increased quantities of hydrogen peroxide, to evaluate potential contribution of p66Shc signaling to renal damage in ischemia reperfusion rat model. Analysis of outer medulla tubule damage revealed the lack of contribution of either p66Shc expression or its constitutive signaling to IR injury in rat model.
登录
查看更多内容
影响因子：
4.8
作者：
Arany, Istvan;Faisal, Amir;Safirstein, Robert L.
通讯作者：
Safirstein, Robert L.
影响因子：
6.1
作者：
Arany, Istvan;Clark, Jeb;Juncos, Luis A.
通讯作者：
Juncos, Luis A.
影响因子：
2.9
作者：
Aksamitiene, Edita;Hoek, Jan B.;Kiyatkin, Anatoly
通讯作者：
Kiyatkin, Anatoly
影响因子：
--
作者：
Zhao, Wen-Yu;Han, Shu;Zeng, Li
通讯作者：
Zeng, Li
影响因子：
3.6
作者：
Allegretti AS;Parada XV;Endres P;Zhao S;Krinsky S;St Hillien SA;Kalim S;Nigwekar SU;Flood JG;Nixon A;Simonetto DA;Juncos LA;Karakala N;Wadei HM;Regner KR;Belcher JM;Nadim MK;Garcia-Tsao G;Velez JCQ;Parikh SM;Chung RT;HRS-HARMONY study investigators
通讯作者：
HRS-HARMONY study investigators