Bax and Bak have critical roles in ischemic acute kidney injury in global and proximal tubule-specific knockout mouse models.
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Autophagy, Innate Immunity and Tissue Repair in Acute Kidney InjuryMitophagy: Basic Mechanism and Potential Role in Kidney DiseasesTherapeutic translation in acute kidney injury: the epithelial/endothelial axisDNA damage response in renal ischemia-reperfusion and ATP-depletion injury of renal tubular cellsOMA1 mediates OPA1 proteolysis and mitochondrial fragmentation in experimental models of ischemic kidney injury.Regulation of necrotic cell death: p53, PARP1 and cyclophilin D-overlapping pathways of regulated necrosis?Changes in metabolic profiles during acute kidney injury and recovery following ischemia/reperfusionDefining the acute kidney injury and repair transcriptomeTargeted deletion of p53 in the proximal tubule prevents ischemic renal injuryRegulated cell death in AKI.Mitochondrial dysregulation and protection in cisplatin nephrotoxicity.Hyperglycemia, p53, and mitochondrial pathway of apoptosis are involved in the susceptibility of diabetic models to ischemic acute kidney injury.mTOR contributes to ER stress and associated apoptosis in renal tubular cellsSirt1 deletion leads to enhanced inflammation and aggravates endotoxin-induced acute kidney injurySUMOylation occurs in acute kidney injury and plays a cytoprotective roleMitochondrial function and disturbances in the septic kidneySimultaneous deletion of Bax and Bak is required to prevent apoptosis and interstitial fibrosis in obstructive nephropathyInhibiting microRNA-449 Attenuates Cisplatin-Induced Injury in NRK-52E Cells Possibly via Regulating the SIRT1/P53/BAX PathwaymiR-146a is essential for lipopolysaccharide (LPS)-induced cross-tolerance against kidney ischemia/reperfusion injury in mice.Heat shock factor 1 induces crystallin-αB to protect against cisplatin nephrotoxicity.Mitochondrial Homeostasis in Acute Organ Failure.Double knockout of Bax and Bak from kidney proximal tubules reduces unilateral urethral obstruction associated apoptosis and renal interstitial fibrosis.Mitochondria-targeted therapies for acute kidney injury.Ischemia as a factor affecting innate immune responses in kidney transplantation.Blocking peptides and molecular mimicry as treatment for kidney disease.Fate of Neutrophils during the Recovery Phase of Ischemia/Reperfusion Induced Acute Kidney Injury.Blocking junctional adhesion molecule C promotes the recovery of cisplatin-induced acute kidney injury.K+ deficiency caused defects in renal tubular cell proliferation, oxidative stress response, tissue repair and tight junction integrity, but enhanced energy production, proteasome function and cellular K+ uptake.Mitochondrial energetics in the kidney.AKI on CKD: heightened injury, suppressed repair, and the underlying mechanisms.Functional Role of SUV39H1 in Human Renal Tubular Epithelial Cells Under High-glucose Ambiance.Effects of hydroxyethyl starch 130/0.4 on the kidney tissue of rats with ureteral obstruction
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Bax and Bak have critical roles in ischemic acute kidney injury in global and proximal tubule-specific knockout mouse models.
description
2013 nî lūn-bûn
@nan
2013年の論文
@ja
2013年論文
@yue
2013年論文
@zh-hant
2013年論文
@zh-hk
2013年論文
@zh-mo
2013年論文
@zh-tw
2013年论文
@wuu
2013年论文
@zh
2013年论文
@zh-cn
name
Bax and Bak have critical role ...... pecific knockout mouse models.
@en
type
label
Bax and Bak have critical role ...... pecific knockout mouse models.
@en
prefLabel
Bax and Bak have critical role ...... pecific knockout mouse models.
@en
P2093
P2860
P356
P1433
P1476
Bax and Bak have critical role ...... pecific knockout mouse models.
@en
P2093
Ganesan Ramesh
Jian-Kang Chen
Qingqing Wei
Zheng Dong
P2860
P2888
P304
P356
10.1038/KI.2013.68
P407
P577
2013-03-06T00:00:00Z
P5875
P6179
1050172524