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Wnt/β-catenin signaling pathway promotes renal ischemia–reperfusion injury through inducing oxidative stress and inflammation response
Journal of Receptors and Signal Transduction ( IF 2.8 ) Pub Date : 2020-06-24 , DOI: 10.1080/10799893.2020.1783555 Qi Dong 1 , Yingxin Jie 2 , Jian Ma 3 , Chen Li 4 , Ting Xin 5 , Dingwei Yang 1
Journal of Receptors and Signal Transduction ( IF 2.8 ) Pub Date : 2020-06-24 , DOI: 10.1080/10799893.2020.1783555 Qi Dong 1 , Yingxin Jie 2 , Jian Ma 3 , Chen Li 4 , Ting Xin 5 , Dingwei Yang 1
Affiliation
Abstract Oxidative stress and inflammation response have been found to be associated with renal ischemia reperfusion (I/R) injury through an undefined mechanism. The aim of our study is to explore the influence of Wnt/β-catenin signaling pathway on oxidative stress and inflammation response during renal I/R injury. The results of our study demonstrated that oxidative stress was induced whereas antioxidative factors were suppressed by renal I/R injury. Besides, the transcriptions and activities of pro-inflammation factors were also upregulated by renal I/R injury. Interestingly, inhibition of Wnt/β-catenin signaling pathway significantly attenuated I/R-mediated oxidative stress and inflammation response. Therefore, our results report a novel pathway responsible for renal I/R injury. Inhibition of Wnt/β-catenin signaling pathway would be considered as an effective approach to regulate oxidative stress and inflammation response in reperfused kidney.
中文翻译:
Wnt/β-catenin信号通路通过诱导氧化应激和炎症反应促进肾缺血再灌注损伤
摘要 氧化应激和炎症反应已被发现与肾缺血再灌注 (I/R) 损伤有关,其机制尚不明确。我们研究的目的是探讨 Wnt/β-catenin 信号通路对肾 I/R 损伤过程中氧化应激和炎症反应的影响。我们的研究结果表明,氧化应激被诱导,而抗氧化因子被肾 I/R 损伤抑制。此外,促炎因子的转录和活性也因肾 I/R 损伤而上调。有趣的是,Wnt/β-catenin 信号通路的抑制显着减弱了 I/R 介导的氧化应激和炎症反应。因此,我们的结果报告了导致肾 I/R 损伤的新途径。
更新日期:2020-06-24
中文翻译:
Wnt/β-catenin信号通路通过诱导氧化应激和炎症反应促进肾缺血再灌注损伤
摘要 氧化应激和炎症反应已被发现与肾缺血再灌注 (I/R) 损伤有关,其机制尚不明确。我们研究的目的是探讨 Wnt/β-catenin 信号通路对肾 I/R 损伤过程中氧化应激和炎症反应的影响。我们的研究结果表明,氧化应激被诱导,而抗氧化因子被肾 I/R 损伤抑制。此外,促炎因子的转录和活性也因肾 I/R 损伤而上调。有趣的是,Wnt/β-catenin 信号通路的抑制显着减弱了 I/R 介导的氧化应激和炎症反应。因此,我们的结果报告了导致肾 I/R 损伤的新途径。