Peritubular capillary loss after mouse acute nephrotoxicity correlates with down-regulation of vascular endothelial growth factor-A and hypoxia-inducible factor-1 alpha. - Wikidata - wikimedia - TriplyDB

Peritubular capillary loss after mouse acute nephrotoxicity correlates with down-regulation of vascular endothelial growth factor-A and hypoxia-inducible factor-1 alpha.

Peritubular capillary loss after mouse acute nephrotoxicity correlates with down-regulation of vascular endothelial growth factor-A and hypoxia-inducible factor-1 alpha.

http://www.wikidata.org/entity/Q35843371

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Hypoxia-based strategies for angiogenic induction: the dawn of a new era for ischemia therapy and tissue regeneration Tipping the balance from angiogenesis to fibrosis in CKD Quantitative Micro-Computed Tomography Imaging of Vascular Dysfunction in Progressive Kidney Diseases Hypoxia-inducible factors in the kidney Severe renal mass reduction impairs recovery and promotes fibrosis after AKI Dysmorphogenesis of kidney cortical peritubular capillaries in angiopoietin-2-deficient mice p53 regulates renal expression of HIF-1{alpha} and pVHL under physiological conditions and after ischemia-reperfusion injury Inhibition of tubulointerstitial fibrosis by pentoxifylline is associated with improvement of vascular endothelial growth factor expression Silencing SMOC2 ameliorates kidney fibrosis by inhibiting fibroblast to myofibroblast transformation Protection of podocytes from hyperhomocysteinemia-induced injury by deletion of the gp91phox gene.Mobilized human hematopoietic stem/progenitor cells promote kidney repair after ischemia/reperfusion injury Pharmacological and genetic depletion of fibrinogen protects from kidney fibrosis.Fluorescence microangiography for quantitative assessment of peritubular capillary changes after AKI in mice Kidney pericytes: roles in regeneration and fibrosis.Acid sphingomyelinase gene knockout ameliorates hyperhomocysteinemic glomerular injury in mice lacking cystathionine-β-synthase Absence of chloride intracellular channel 4 (CLIC4) predisposes to acute kidney injury but has minimal impact on recovery Models of chronic kidney disease Impaired endothelial proliferation and mesenchymal transition contribute to vascular rarefaction following acute kidney injury.Vascular homeostasis and angiogenesis determine therapeutic effectiveness in type 2 diabetes.MMP-9 gene deletion mitigates microvascular loss in a model of ischemic acute kidney injury.Attenuation of folic acid-induced renal inflammatory injury in platelet-activating factor receptor-deficient mice N-acetylcysteine is effective for prevention but not for treatment of folic acid-induced acute kidney injury in mice Investigating mechanisms of chronic kidney disease in mouse models The p53 inhibitor pifithrin-α can stimulate fibrosis in a rat model of ischemic acute kidney injury.Early loss of peritubular capillaries after kidney transplantation.Current understanding of HIF in renal disease.Intrarenal oxygenation in chronic renal failure.Renal expression of hypoxia inducible factor-1α in patients with chronic kidney disease: a clinicopathologic study from nephrectomized kidneys Long-term High Salt Diet Causes Hypertension and Decreases Renal Expression of Vascular Endothelial Growth Factor in Sprague-Dawley Rats.Pre-existing renal disease promotes sepsis-induced acute kidney injury and worsens outcome Urinary excretion of liver type fatty acid binding protein accurately reflects the degree of tubulointerstitial damage.Abnormal angiogenesis in diabetic nephropathy.Localized immunosuppressive environment in the foreign body response to implanted biomaterials.Vascular endothelial growth factor receptor inhibitor enhances dietary salt-induced hypertension in Sprague-Dawley rats.Intrapulmonary delivery of XCL1-targeting small interfering RNA in mice chronically infected with Mycobacterium tuberculosis Influence of the Expression of Inflammatory Markers on Kidney after Fetal Programming in an Experimental Model of Renal Failure.Pathophysiology of acute kidney injury Selective iNOS inhibition for the treatment of sepsis-induced acute kidney injury.Suppressed mitochondrial biogenesis in folic acid-induced acute kidney injury and early fibrosis.Capillary dilation and rarefaction are correlated with intracapillary inflammation in antibody-mediated rejection.

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P2860

Peritubular capillary loss after mouse acute nephrotoxicity correlates with down-regulation of vascular endothelial growth factor-A and hypoxia-inducible factor-1 alpha.

http://www.wikidata.org/entity/Q35843371

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2003 nî lūn-bûn

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2003年學術文章

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Peritubular capillary loss aft ...... oxia-inducible factor-1 alpha.

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Hai-Tao Yuan

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Jolanta E Pitera

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Xiao-Zhong Li

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Endothelial PAS domain protein 1 (EPAS1), a transcription factor selectively expressed in endothelial cells

A novel bHLH-PAS factor with close sequence similarity to hypoxia-inducible factor 1alpha regulates the VEGF expression and is potentially involved in lung and vascular development

Cellular and developmental control of O2 homeostasis by hypoxia-inducible factor 1 alpha

Proliferation and remodeling of the peritubular microcirculation after nephron reduction: association with the progression of renal lesions

Differential expression of Tie-2 receptors and angiopoietins in response to in vivo hypoxia in rats

Determination of hypoxic region by hypoxia marker in developing mouse embryos in vivo: a possible signal for vessel development.

Cell biology and molecular mechanisms of injury in ischemic acute renal failure.

Molecular mechanisms of blood vessel growth.

Role of the microvascular endothelium in progressive renal disease.

pVHL19 is a biologically active product of the von Hippel-Lindau gene arising from internal translation initiation

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