Reduced Lipid Peroxidation and Ischemia-Reperfusion Injury after Lung Transplantation Using Low-Potassium Dextran Solution for Lung Preservation

1997 ◽  
Vol 156 (4) ◽  
pp. 1073-1081 ◽  
Author(s):  
FUMIO SAKAMAKI ◽  
HANS HOFFMANN ◽  
CHRISTIAN MÜLLER ◽  
HENDRIK DIENEMANN ◽  
KONRAD MESSMER ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Lung Transplantation ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Lung Preservation ◽  
Low Potassium ◽  
Dextran Solution

Pilot Trial of Extended Hypothermic Lung Preservation to Analyze Ischemia-reperfusion Injury in Pigs

2021 ◽  
Vol 57 (7) ◽  
pp. 479-489
Author(s):  
Amaia Ojanguren ◽  
Maite Santamaría ◽  
Lucía Milla-Collado ◽  
Carlos Fraile ◽  
Sonia Gatius-Calderó ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Pilot Trial ◽  
Lung Preservation

Lipid Peroxidation Activates Mitogen-Activated Protein Kinases in Testicular Ischemia-Reperfusion Injury

2006 ◽  
Vol 176 (4) ◽  
pp. 1666-1672 ◽  
Author(s):  
Pietro Antonuccio ◽  
Letteria Minutoli ◽  
Carmelo Romeo ◽  
Piero Antonio Nicòtina ◽  
Alessandra Bitto ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Reperfusion Injury ◽  
Protein Kinases ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Mitogen Activated Protein Kinases ◽  
Mitogen Activated Protein ◽  
Testicular Ischemia

CCR2 Deficiency Attenuates Ischemia Reperfusion Injury After Lung Transplantation

2011 ◽  
Vol 165 (2) ◽  
pp. 331
Author(s):  
R.G. Nava ◽  
A.C. Bribriesco ◽  
W. Li ◽  
A.E. Gelman ◽  
A.S. Krupnick ◽  
...  
Keyword(s):  
Lung Transplantation ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion

Expression of Claudin-4 in Lung Ischemia-Reperfusion Injury in Experimental Lung Transplantation

2020 ◽  
pp. 1-10
Author(s):  
Antonia Luna-Flores ◽  
J. Raúl Olmos-Zuñiga ◽  
Rogelio Jasso-Victoria ◽  
Miguel Gaxiola-Gaxiola ◽  
Teresa Aguirre-Pérez ◽  
...  
Keyword(s):  
Lung Transplantation ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion

scholarly journals Cell Death Patterns Due to Warm Ischemia or Reperfusion in Renal Tubular Epithelial Cells Originating from Human, Mouse, or the Native Hibernator Hamster

Biology ◽  
2018 ◽  
Vol 7 (4) ◽  
pp. 48 ◽  
Author(s):  
Theodoros Eleftheriadis ◽  
Georgios Pissas ◽  
Georgia Antoniadi ◽  
Vassilios Liakopoulos ◽  
Ioannis Stefanidis
Keyword(s):  
Lipid Peroxidation ◽  
Acute Kidney Injury ◽  
Cell Death ◽  
Epithelial Cells ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Kidney Injury ◽  
Human Cells ◽  
Tubular Epithelial Cells

Ischemia–reperfusion injury contributes to the pathogenesis of many diseases, with acute kidney injury included. Hibernating mammals survive prolonged bouts of deep torpor with a dramatic drop in blood pressure, heart, and breathing rates, interspersed with short periods of arousal and, consequently, ischemia–reperfusion injury. Clarifying the differences under warm anoxia or reoxygenation between human cells and cells from a native hibernator may reveal interventions for rendering human cells resistant to ischemia–reperfusion injury. Human and hamster renal proximal tubular epithelial cells (RPTECs) were cultured under warm anoxia or reoxygenation. Mouse RPTECs were used as a phylogenetic control for hamster cells. Cell death was assessed by both cell imaging and lactate dehydrogenase (LDH) release assay, apoptosis by cleaved caspase-3, autophagy by microtubule-associated protein 1-light chain 3 B II (LC3B-II) to LC3B-I ratio, necroptosis by phosphorylated mixed-lineage kinase domain-like pseudokinase, reactive oxygen species (ROS) fluorometrically, and lipid peroxidation, the end-point of ferroptosis, by malondialdehyde. Human cells died after short periods of warm anoxia or reoxygenation, whereas hamster cells were extremely resistant. In human cells, apoptosis contributed to cell death under both anoxia and reoxygenation. Although under reoxygenation, ROS increased in both human and hamster RPTECs, lipid peroxidation-induced cell death was detected only in human cells. Autophagy was observed only in human cells under both conditions. Necroptosis was not detected in any of the evaluated cells. Clarifying the ways that are responsible for hamster RPTECs escaping from apoptosis and lipid peroxidation-induced cell death may reveal interventions for preventing ischemia–reperfusion-induced acute kidney injury in humans.

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