scholarly journals Correction: Dendritic Cell Sphingosine 1-Phosphate Receptor-3 Regulates Th1-Th2 Polarity in Kidney Ischemia-Reperfusion Injury

2012 ◽  
Vol 189 (9) ◽  
pp. 4696-4696
Author(s):  
Amandeep Bajwa ◽  
Liping Huang ◽  
Hong Ye ◽  
Krishna Dondeti ◽  
Steven Song ◽  
...  
Keyword(s):  
Dendritic Cell ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Sphingosine 1 Phosphate ◽  
Kidney Ischemia

scholarly journals Dendritic Cell Sphingosine 1-Phosphate Receptor-3 Regulates Th1–Th2 Polarity in Kidney Ischemia–Reperfusion Injury

2012 ◽  
Vol 189 (5) ◽  
pp. 2584-2596 ◽  
Author(s):  
Amandeep Bajwa ◽  
Liping Huang ◽  
Hong Ye ◽  
Krishna Dondeti ◽  
Steven Song ◽  
...  
Keyword(s):  
Dendritic Cell ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Sphingosine 1 Phosphate ◽  
Kidney Ischemia

scholarly journals Selective deletion of the endothelial sphingosine-1-phosphate 1 receptor exacerbates kidney ischemia–reperfusion injury

2014 ◽  
Vol 85 (4) ◽  
pp. 807-823 ◽  
Author(s):  
Ahrom Ham ◽  
Mihwa Kim ◽  
Joo Yun Kim ◽  
Kevin M. Brown ◽  
Marcus Fruttiger ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Sphingosine 1 Phosphate ◽  
Kidney Ischemia

scholarly journals Mitochondria-Targeted Antioxidants: Future Perspectives in Kidney Ischemia Reperfusion Injury

2016 ◽  
Vol 2016 ◽  
pp. 1-12 ◽  
Author(s):  
Aleksandra Kezic ◽  
Ivan Spasojevic ◽  
Visnja Lezaic ◽  
Milica Bajcetic
Keyword(s):  
Oxidative Stress ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Myocardial Infarct ◽  
Ischemia Reperfusion ◽  
Current Status ◽  
Long Time ◽  
Myocardial Ischemia Reperfusion Injury ◽  
Myocardial Ischemia Reperfusion ◽  
Kidney Ischemia

Kidney ischemia/reperfusion injury emerges in various clinical settings as a great problem complicating the course and outcome. Ischemia/reperfusion injury is still an unsolved puzzle with a great diversity of investigational approaches, putting the focus on oxidative stress and mitochondria. Mitochondria are both sources and targets of ROS. They participate in initiation and progression of kidney ischemia/reperfusion injury linking oxidative stress, inflammation, and cell death. The dependence of kidney proximal tubule cells on oxidative mitochondrial metabolism makes them particularly prone to harmful effects of mitochondrial damage. The administration of antioxidants has been used as a way to prevent and treat kidney ischemia/reperfusion injury for a long time. Recently a new method based on mitochondria-targeted antioxidants has become the focus of interest. Here we review the current status of results achieved in numerous studies investigating these novel compounds in ischemia/reperfusion injury which specifically target mitochondria such as MitoQ, Szeto-Schiller (SS) peptides (Bendavia), SkQ1 and SkQR1, and superoxide dismutase mimics. Based on the favorable results obtained in the studies that have examined myocardial ischemia/reperfusion injury, ongoing clinical trials investigate the efficacy of some novel therapeutics in preventing myocardial infarct. This also implies future strategies in preventing kidney ischemia/reperfusion injury.

Inhibition of kidney ischemia–reperfusion injury through local infusion of a TLR2 blocker

2014 ◽  
Vol 407 ◽  
pp. 146-150 ◽  
Author(s):  
Hye J. Kim ◽  
Sang J. Park ◽  
Sumi Koo ◽  
Hee J. Cha ◽  
Jong S. Lee ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Kidney Ischemia

Splenectomy Attenuates the Course of Kidney Ischemia-Reperfusion Injury in Rats

2014 ◽  
Vol 46 (8) ◽  
pp. 2558-2561 ◽  
Author(s):  
W. Wystrychowski ◽  
L. Filipczyk ◽  
L. Cierpka ◽  
E. Obuchowicz ◽  
A. Więcek ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Kidney Ischemia
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