Phenotype and influx kinetics of leukocytes and inflammatory cytokine production in kidney ischemia/reperfusion injury

Nephrology ◽  
2017 ◽  
Vol 23 (1) ◽  
pp. 75-85 ◽  
Author(s):  
Timothy M. Williams ◽  
Andrea F. Wise ◽  
Daniel S. Layton ◽  
Sharon D. Ricardo
Keyword(s):  
Reperfusion Injury ◽  
Inflammatory Cytokine ◽  
Cytokine Production ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Inflammatory Cytokine Production ◽  
Kinetics Of ◽  
Influx Kinetics ◽  
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.

scholarly journals Enhancer of zeste homolog 2 modulates oxidative stress‐mediated pyroptosis in vitro and in a mouse kidney ischemia‐reperfusion injury model

2019 ◽  
Vol 34 (1) ◽  
pp. 835-852 ◽  
Author(s):  
Hao Liu ◽  
Zhiyuan Chen ◽  
Xiaodong Weng ◽  
Hui Chen ◽  
Yang Du ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Mouse Kidney ◽  
Injury Model ◽  
Enhancer Of Zeste ◽  
Kidney Ischemia

scholarly journals Reducing Inflammatory Cytokine Production from Renal Collecting Duct Cells by Inhibiting GATA2 Ameliorates Acute Kidney Injury

2017 ◽  
Vol 37 (22) ◽  
Author(s):  
Lei Yu ◽  
Takashi Moriguchi ◽  
Hiroshi Kaneko ◽  
Makiko Hayashi ◽  
Atsushi Hasegawa ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Inflammatory Cytokines ◽  
Inflammatory Cytokine ◽  
Cytokine Production ◽  
Ischemia Reperfusion Injury ◽  
Collecting Duct ◽  
Ischemia Reperfusion ◽  
Kidney Injury ◽  
Cytokine Gene Expression ◽  
Renal Tubular Cell

ABSTRACT Acute kidney injury (AKI) is a leading cause of chronic kidney disease. Proximal tubules are considered to be the primary origin of pathogenic inflammatory cytokines in AKI. However, it remains unclear whether other cell types, including collecting duct (CD) cells, participate in inflammatory processes. The transcription factor GATA2 is specifically expressed in CD cells and maintains their cellular identity. To explore the pathophysiological function of GATA2 in AKI, we generated renal tubular cell-specific Gata2 deletion (G2CKO) mice and examined their susceptibility to ischemia reperfusion injury (IRI). Notably, G2CKO mice exhibited less severe kidney damage, with reduced granulomacrophagic infiltration upon IRI. Transcriptome analysis revealed that a series of inflammatory cytokine genes were downregulated in GATA2-deficient CD cells, suggesting that GATA2 induces inflammatory cytokine expression in diseased kidney CD cells. Through high-throughput chemical library screening, we identified a potent GATA inhibitor. The chemical reduces cytokine production in CD cells and protects the mouse kidney from IRI. These results revealed a novel pathological mechanism of renal IRI, namely, that CD cells produce inflammatory cytokines and promote IRI progression. In injured kidney CD cells, GATA2 exerts a proinflammatory function by upregulating inflammatory cytokine gene expression. GATA2 can therefore be considered a therapeutic target for AKI.

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

Effect of tourniquet use during total knee arthroplasty on global inflammatory cytokine changes associated with ischemia- reperfusion injury

2017 ◽  
Vol 2 (1) ◽  
pp. 1
Author(s):  
ETodd Schroeder ◽  
Brian Wu ◽  
Ryan Graff ◽  
Ido Badash ◽  
JosephG Skeate ◽  
...  
Keyword(s):  
Total Knee Arthroplasty ◽  
Reperfusion Injury ◽  
Knee Arthroplasty ◽  
Inflammatory Cytokine ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Total Knee

The Toll-IL-1R Member Tir8 Modulates Post-Transplant Kidney Ischemia/reperfusion Injury By Inhibiting Resident F4/80+CX3CR1+ Cell Expansion.

2014 ◽  
Vol 98 ◽  
pp. 38
Author(s):  
P. Cassis ◽  
S. Solini ◽  
N. Azzollini ◽  
G. Remuzzi ◽  
M. Noris ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Cell Expansion ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Post Transplant ◽  
Transplant Kidney ◽  
Kidney Ischemia
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