Redox dependence of glomerular epithelial cell hypertrophy in response to glucose. - Wikidata - awgldk - TriplyDB

Redox dependence of glomerular epithelial cell hypertrophy in response to glucose.

Redox dependence of glomerular epithelial cell hypertrophy in response to glucose.

http://www.wikidata.org/entity/Q46761417

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Podocytes Drug Targets for Oxidative Podocyte Injury in Diabetic Nephropathy Ribosomal biogenesis induction by high glucose requires activation of upstream binding factor in kidney glomerular epithelial cells Effects of the antioxidant drug tempol on renal oxygenation in mice with reduced renal mass.Astragaloside IV, a novel antioxidant, prevents glucose-induced podocyte apoptosis in vitro and in vivo.2,3',4,5'-Tetramethoxystilbene prevents deoxycorticosterone-salt-induced hypertension: contribution of cytochrome P-450 1B1 Canonical transient receptor potential channels in diabetes.CXCL16 and oxLDL are induced in the onset of diabetic nephropathy.Protective effects of leukemia inhibitory factor against oxidative stress during high glucose-induced apoptosis in podocytes.Cytochrome P450 1B1 gene disruption minimizes deoxycorticosterone acetate-salt-induced hypertension and associated cardiac dysfunction and renal damage in mice.Mechanism of oxidative DNA damage in diabetes: tuberin inactivation and downregulation of DNA repair enzyme 8-oxo-7,8-dihydro-2'-deoxyguanosine-DNA glycosylase Mechanisms of podocyte injury in diabetes: role of cytochrome P450 and NADPH oxidases.Nox4-derived reactive oxygen species mediate cardiomyocyte injury in early type 1 diabetes Nephropathy and elevated BP in mice with podocyte-specific NADPH oxidase 5 expression.Oxidative stress, Nox isoforms and complications of diabetes--potential targets for novel therapies.Renin-angiotensin system within the diabetic podocyte.Role of Protein Kinase G and Reactive Oxygen Species in the Regulation of Podocyte Function in Health and Disease.Research Progress on Mechanism of Podocyte Depletion in Diabetic Nephropathy.Interplay between the Notch and PI3K/Akt pathways in high glucose-induced podocyte apoptosis.Heat shock response protects human peritoneal mesothelial cells from dialysate-induced oxidative stress and mitochondrial injury.Potential role of branched-chain amino acids in glucose metabolism through the accelerated induction of the glucose-sensing apparatus in the liver.

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P2860

Redox dependence of glomerular epithelial cell hypertrophy in response to glucose.

http://www.wikidata.org/entity/Q46761417

description

2005 nî lūn-bûn

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2005年の論文

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2005年学术文章

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2005年学术文章

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2005年学术文章

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2005年学术文章

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2005年学术文章

@zh-my

2005年学术文章

@zh-sg

2005年學術文章

@yue

2005年學術文章

@zh-hant

name

Redox dependence of glomerular epithelial cell hypertrophy in response to glucose.

@en

Redox dependence of glomerular epithelial cell hypertrophy in response to glucose.

@nl

type

label

Redox dependence of glomerular epithelial cell hypertrophy in response to glucose.

@en

Redox dependence of glomerular epithelial cell hypertrophy in response to glucose.

@nl

prefLabel

Redox dependence of glomerular epithelial cell hypertrophy in response to glucose.

@en

Redox dependence of glomerular epithelial cell hypertrophy in response to glucose.

@nl

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AJPRENAL.00313.2005

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American Journal of Physiology - Renal Physiology

P1476

Redox dependence of glomerular epithelial cell hypertrophy in response to glucose.

@en

P2093

Basant Bhandari

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Goutam Ghosh Choudhury

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Hanna E Abboud

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Hernan Rincon-Choles

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Nam-Ho Kim

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P2860

Free radicals in the physiological control of cell function

Activation of phosphoinositide 3-kinase in response to high glucose leads to regulation of reactive oxygen species-related nuclear factor-kappaB activation and cyclooxygenase-2 expression in mesangial cells

Angiotensin II receptor blocker inhibits p27Kip1 expression in glucose-stimulated podocytes and in diabetic glomeruli

Angiotensin II-induced ERK1/ERK2 activation and protein synthesis are redox-dependent in glomerular mesangial cells

The pathobiology of diabetic complications: a unifying mechanism

The intrarenal renin-angiotensin system and diabetic nephropathy.

Angiotensin II type 1 receptor overexpression in podocytes induces glomerulosclerosis in transgenic rats.

High glucose induces human endothelial cell apoptosis through a phosphoinositide 3-kinase-regulated cyclooxygenase-2 pathway.

Phosphatidylinositol 3-kinase-mediated effects of glucose on vacuolar H+-ATPase assembly, translocation, and acidification of intracellular compartments in renal epithelial cells.

Molecular mechanisms of diabetic renal hypertrophy.

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10.1152/AJPRENAL.00313.2005

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