Manganese porphyrin reduces renal injury and mitochondrial damage during ischemia/reperfusion
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Reduction in mitochondrial iron alleviates cardiac damage during injury
Excess cellular iron increases reactive oxygen species (ROS) production and causes cellular damage. Mitochondria are the major site of iron metabolism and ROS production; however, few studies have investigated the role of mitochondrial iron in the development of cardiac disorders, such as ischemic heart disease or cardiomyopathy (CM). We observe increased mitochondrial iron in mice after ischem...
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Atypical hemolytic uremic syndrome (aHUS) is a genetic, life-threatening disease characterized by uncontrolled complement activation, systemic thrombotic microangiopathy (TMA), and vital organ damage. We evaluated the effect of terminal complement blockade with the anti-C5 monoclonal antibody eculizumab on biomarkers of cellular processes involved in TMA in patients with aHUS longitudinally, du...
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BACKGROUND Reactive oxygen species (ROS) play a major role in causing injury in ischemia-reperfusion (I/R). Mitochondrial DNA (mtDNA) is particularly vulnerable to oxidative damage. We propose that increased mitochondrial ROS production is likely to damage mtDNA, causing further injury to mitochondria, and postconditioning (POC) may ameliorate kidney I/R injury by mitigating mitochondrial damag...
متن کاملMitoQ Blunts Mitochondrial and Renal Damage during Cold Preservation of Porcine Kidneys
Cold preservation has greatly facilitated the use of cadaveric kidneys for transplantation but damage occurs during the preservation episode. It is well established that oxidant production increases during cold renal preservation and mitochondria are a key target for injury. Our laboratory has demonstrated that cold storage of renal cells and rat kidneys leads to increased mitochondrial superox...
متن کاملChymase Mediates Injury and Mitochondrial Damage in Cardiomyocytes during Acute Ischemia/Reperfusion in the Dog
Cardiac ischemia and reperfusion (I/R) injury occurs because the acute increase in oxidative/inflammatory stress during reperfusion culminates in the death of cardiomyocytes. Currently, there is no drug utilized clinically that attenuates I/R injury in patients. Previous studies have demonstrated degranulation of mast cell contents into the interstitium after I/R. Using a dog model of I/R, we t...
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ژورنال
عنوان ژورنال: Free Radical Biology and Medicine
سال: 2007
ISSN: 0891-5849
DOI: 10.1016/j.freeradbiomed.2007.02.016