2020
DOI: 10.3390/antiox9080769
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Abstract: Ischemia/reperfusion (I/R) is one of the major causes of acute kidney injury (AKI) and associated with increased mortality and progression to chronic kidney injury (CKI). Molecular mechanisms underlying I/R injury involve the production and excessive accumulation of reactive oxygen species (ROS). Peroxiredoxin (Prx) V, a cysteine-dependent peroxidase, is located in the cytosol, mitochondria, and peroxisome and has an intensive ROS scavenging activity. Therefore, we focused on the role of Prx V during I/R-induc… Show more

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Cited by 7 publications
(5 citation statements)
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“…As apocynin is experimentally used as an inhibitor of vascular NADPH oxidase, and is known as an antioxidant [ 44 ], it is reasonable to assume that apocynin treatment will reduce the level of superoxide anion and improve tissue integrity. Many antioxidant enzymes maintain an appropriate level of ROS and prevent oxidative damages [ 45 ]. Additionally, HBO preconditioning may ameliorate creatinine and phosphate clearances in postischemic AKI by upregulation of antioxidant enzymes activities [ 46 , 47 ].…”
Section: Discussionmentioning
confidence: 99%
“…As apocynin is experimentally used as an inhibitor of vascular NADPH oxidase, and is known as an antioxidant [ 44 ], it is reasonable to assume that apocynin treatment will reduce the level of superoxide anion and improve tissue integrity. Many antioxidant enzymes maintain an appropriate level of ROS and prevent oxidative damages [ 45 ]. Additionally, HBO preconditioning may ameliorate creatinine and phosphate clearances in postischemic AKI by upregulation of antioxidant enzymes activities [ 46 , 47 ].…”
Section: Discussionmentioning
confidence: 99%
“…As expected, I-Prx V was found in the mitochondrial but not cytosolic fraction. The adrenal gland is an organ where physical stress induces corticosterone steroidogenesis and consequently H 2 O 2 production, followed by a slow conversion of active Prx III-SH to inactive Prx III-SO 2 H. Immobilization stress for 1 hr resulted in an increase in the amount of I-Prx V that peaked at 4 hr and diminished thereafter, as well as a steady decrease in the amount of S-Prx V. Furthermore we previously showed that mitochondrial S-Prx V in kidney was significantly reduced when mice were subjected to renal ischemia/reperfusion injury, which is accompanied by mitochondrial ROS production [24]. Together, these in vivo experiments support the notion that MIP is inhibited by mitochondrially produced H 2 O 2 .…”
Section: Discussionmentioning
confidence: 90%
“…Prx V KO mice were as described previously [24]. Srx KO mice, in which Srx is ablated specifically in steroidogenic tissues, were also described previously [25].…”
Section: Animals and Antibodiesmentioning
confidence: 99%
“…Prdx5 deficiency induces a susceptibility to high-fat diet-induced obesity and associated metabolic disorders [ 109 ]. Moreover, the depletion of Prdx5 significantly augmented kidney inflammation after renal ischemia–reperfusion injury [ 110 ]. Notably, extracellular Prdx5 is the strongest contributor among all Prdx isoforms to induce the expression of inflammatory cytokines through Toll-like receptor (TLR) 2 and TLR4 after a postischemic brain injury via damage-associated molecular patterns [ 111 ].…”
Section: Prdxs In Cvdmentioning
confidence: 99%