Activation of p53 promotes renal injury in acute aristolochic acid nephropathy.
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The restrained expression of NF-kB in renal tissue ameliorates folic acid induced acute kidney injury in miceAn Integrated View of Aristolochic Acid Nephropathy: Update of the LiteraturePathogenesis of acute kidney injury: foundation for clinical practice.Relaxin attenuates aristolochic acid induced human tubular epithelial cell apoptosis in vitro by activation of the PI3K/Akt signaling pathway.miR-192 mediates TGF-beta/Smad3-driven renal fibrosis.Tubular p53 regulates multiple genes to mediate AKIEvaluating weight of evidence in the mystery of Balkan endemic nephropathy.Dynamic multiphoton microscopy: focusing light on acute kidney injury.Targeted deletion of p53 in the proximal tubule prevents ischemic renal injuryRenal liver-type fatty acid binding protein (L-FABP) attenuates acute kidney injury in aristolochic acid nephrotoxicity.Hyperglycemia, p53, and mitochondrial pathway of apoptosis are involved in the susceptibility of diabetic models to ischemic acute kidney injury.Role of microRNA 1207-5P and its host gene, the long non-coding RNA Pvt1, as mediators of extracellular matrix accumulation in the kidney: implications for diabetic nephropathyCell cycle arrest and the evolution of chronic kidney disease from acute kidney injury.Loss of tumour suppressor PTEN expression in renal injury initiates SMAD3- and p53-dependent fibrotic responsesMicroRNAs and the glomerulusA microRNA circuit mediates transforming growth factor-β1 autoregulation in renal glomerular mesangial cellsThe p53 inhibitor pifithrin-α can stimulate fibrosis in a rat model of ischemic acute kidney injury.MicroRNA circuits in transforming growth factor-β actions and diabetic nephropathy.Prediction and Characterisation of the System Effects of Aristolochic Acid: A Novel Joint Network Analysis towards Therapeutic and Toxicological Mechanisms.p53 is renoprotective after ischemic kidney injury by reducing inflammation.Amelioration of albuminuria in ROCK1 knockout mice with streptozotocin-induced diabetic kidney diseaseRenal pro-apoptotic proteins are reduced by growth hormone resistance but not by visceral fat removal.Decreased levels of proapoptotic factors and increased key regulators of mitochondrial biogenesis constitute new potential beneficial features of long-lived growth hormone receptor gene-disrupted mice.Transforming growth factor-β-induced cross talk between p53 and a microRNA in the pathogenesis of diabetic nephropathyNumb contributes to renal fibrosis by promoting tubular epithelial cell cycle arrest at G2/Mp53 activates miR-192-5p to mediate vancomycin induced AKIBioinformatics facilitating the use of microarrays to delineate potential miRNA biomarkers in aristolochic acid nephropathy.A PTBA small molecule enhances recovery and reduces postinjury fibrosis after aristolochic acid-induced kidney injury.TGF-β1 → SMAD/p53/USF2 → PAI-1 transcriptional axis in ureteral obstruction-induced renal fibrosis.Naturally occurring aristolochic acid analogues and their toxicities.Aristolochic acid nephropathy: epidemiology, clinical presentation, and treatment.Cell cycle control in the kidney.Mechanisms of maladaptive repair after AKI leading to accelerated kidney ageing and CKD.Renal Protective Effects of 17β-Estradiol on Mice with Acute Aristolochic Acid Nephropathy.Aristolochic acid-induced apoptosis and G2 cell cycle arrest depends on ROS generation and MAP kinases activation.Glutamate dehydrogenase requirement for apoptosis induced by aristolochic acid in renal tubular epithelial cells.Autophagy inhibitors promoted aristolochic acid I induced renal tubular epithelial cell apoptosis via mitochondrial pathway but alleviated nonapoptotic cell death in mouse acute aritolochic acid nephropathy model.Extracellular Signal-Regulated Kinase 1/2 Regulates Mouse Kidney Injury Molecule-1 Expression Physiologically and Following Ischemic and Septic Renal Injury.Endothelial STAT3 Modulates Protective Mechanisms in a Mouse Ischemia-Reperfusion Model of Acute Kidney Injury.TGF-β1/p53 signaling in renal fibrogenesis.
P2860
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P2860
Activation of p53 promotes renal injury in acute aristolochic acid nephropathy.
description
2009 nî lūn-bûn
@nan
2009 թուականի Նոյեմբերին հրատարակուած գիտական յօդուած
@hyw
2009 թվականի նոյեմբերին հրատարակված գիտական հոդված
@hy
2009年の論文
@ja
2009年論文
@yue
2009年論文
@zh-hant
2009年論文
@zh-hk
2009年論文
@zh-mo
2009年論文
@zh-tw
2009年论文
@wuu
name
Activation of p53 promotes renal injury in acute aristolochic acid nephropathy.
@ast
Activation of p53 promotes renal injury in acute aristolochic acid nephropathy.
@en
Activation of p53 promotes renal injury in acute aristolochic acid nephropathy.
@nl
type
label
Activation of p53 promotes renal injury in acute aristolochic acid nephropathy.
@ast
Activation of p53 promotes renal injury in acute aristolochic acid nephropathy.
@en
Activation of p53 promotes renal injury in acute aristolochic acid nephropathy.
@nl
prefLabel
Activation of p53 promotes renal injury in acute aristolochic acid nephropathy.
@ast
Activation of p53 promotes renal injury in acute aristolochic acid nephropathy.
@en
Activation of p53 promotes renal injury in acute aristolochic acid nephropathy.
@nl
P2093
P2860
P356
P1476
Activation of p53 promotes renal injury in acute aristolochic acid nephropathy.
@en
P2093
P2860
P356
10.1681/ASN.2008111133
P50
P577
2009-11-05T00:00:00Z