Lowering blood pressure blocks mesangiolysis and mesangial nodules, but not tubulointerstitial injury, in diabetic eNOS knockout mice. - Wikidata - awgldk - TriplyDB

Lowering blood pressure blocks mesangiolysis and mesangial nodules, but not tubulointerstitial injury, in diabetic eNOS knockout mice.

Lowering blood pressure blocks mesangiolysis and mesangial nodules, but not tubulointerstitial injury, in diabetic eNOS knockout mice.

http://www.wikidata.org/entity/Q41827523

about

Activated CD47 regulates multiple vascular and stress responses: implications for acute kidney injury and its management Midkine and the kidney: health and diseases Midkine in nephrogenesis, hypertension and kidney diseases eNOS knockout mice with advanced diabetic nephropathy have less benefit from renin-angiotensin blockade than from aldosterone receptor antagonists.Podocyte-specific VEGF-a gain of function induces nodular glomerulosclerosis in eNOS null mice.Thrombospondin-1 supports blood pressure by limiting eNOS activation and endothelial-dependent vasorelaxation Role of endothelial nitric oxide synthase in diabetic nephropathy: lessons from diabetic eNOS knockout mice BTBR Ob/Ob mutant mice model progressive diabetic nephropathy.A modest decrease in endothelial NOS in mice comparable to that associated with human NOS3 variants exacerbates diabetic nephropathy Blockade of TSP1-dependent TGF-β activity reduces renal injury and proteinuria in a murine model of diabetic nephropathy.Diffuse glomerular nodular lesions in diabetic pigs carrying a dominant-negative mutant hepatocyte nuclear factor 1-alpha, an inheritant diabetic gene in humans.Role of blood pressure and the renin-angiotensin system in development of diabetic nephropathy (DN) in eNOS-/- db/db mice.Nicorandil as a novel therapy for advanced diabetic nephropathy in the eNOS-deficient mouse.Aberrant production of extracellular matrix proteins and dysfunction in kidney endothelial cells with a short duration of diabetes Thrombospondin 1 mediates renal dysfunction in a mouse model of high-fat diet-induced obesity.Abnormal angiogenesis in diabetic nephropathy.Effect of lowering uric acid on renal disease in the type 2 diabetic db/db mice.Low protein diet inhibits uric acid synthesis and attenuates renal damage in streptozotocin-induced diabetic rats.Endothelial dysfunction as a potential contributor in diabetic nephropathy.The renal endothelium in diabetic nephropathy.Cell biology of diabetic nephropathy: Roles of endothelial cells, tubulointerstitial cells and podocytes Elevated tissue factor expression contributes to exacerbated diabetic nephropathy in mice lacking eNOS fed a high fat diet.Soluble Flt-1 gene therapy ameliorates albuminuria but accelerates tubulointerstitial injury in diabetic mice.Heparan sulfate 6-O-endosulfatases, Sulf1 and Sulf2, regulate glomerular integrity by modulating growth factor signaling.

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P2860

Lowering blood pressure blocks mesangiolysis and mesangial nodules, but not tubulointerstitial injury, in diabetic eNOS knockout mice.

http://www.wikidata.org/entity/Q41827523

description

2009 nî lūn-bûn

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2009年の論文

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2009年論文

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2009年論文

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2009年論文

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2009年論文

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2009年論文

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2009年论文

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2009年论文

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2009年论文

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name

Lowering blood pressure blocks ...... n diabetic eNOS knockout mice.

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The American Journal of Pathology

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Lowering blood pressure blocks ...... in diabetic eNOS knockout mice

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Byron P Croker

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Li Zhang

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Marcelo Heinig

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Maria B Grant

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Mark A Atkinson

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Mark S Segal

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Qiuhong Li

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Takahiko Nakagawa

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Takahiro Nakayama

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Thomas Connor

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P2860

Thrombospondin-1 is an endogenous activator of TGF-beta in experimental diabetic nephropathy in vivo.

A new model of renal microvascular endothelial injury.

Evolving strategies for renoprotection: diabetic nephropathy.

Subtle acquired renal injury as a mechanism of salt-sensitive hypertension.

Growth factor midkine is involved in the pathogenesis of diabetic nephropathy.

Long-term prevention of renal insufficiency, excess matrix gene expression, and glomerular mesangial matrix expansion by treatment with monoclonal antitransforming growth factor-beta antibody in db/db diabetic mice.

Deficiency of endothelial nitric-oxide synthase confers susceptibility to diabetic nephropathy in nephropathy-resistant inbred mice.

Role of VEGF in maintaining renal structure and function under normotensive and hypertensive conditions

Interaction of insulin with the renal proximal tubular cell.

Elevated glucose induction of thrombospondin-1 up-regulates fibronectin synthesis in proximal renal tubular epithelial cells through TGF-beta1 dependent and TGF-beta1 independent pathways.

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Martha Campbell-Thompson

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24043886

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