eNOS deficiency predisposes podocytes to injury in diabetes. - Wikidata - awgldk - TriplyDB

eNOS deficiency predisposes podocytes to injury in diabetes.

eNOS deficiency predisposes podocytes to injury in diabetes.

http://www.wikidata.org/entity/Q36352132

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Crosstalk in glomerular injury and repair Mitochondria, endothelial cell function, and vascular diseases.Phosphodiesterase 5 inhibition ameliorates angiontensin II-induced podocyte dysmotility via the protein kinase G-mediated downregulation of TRPC6 activity.EP4 inhibition attenuates the development of diabetic and non-diabetic experimental kidney disease.Podocytes, signaling pathways, and vascular factors in diabetic kidney disease MicroRNA-29a promotion of nephrin acetylation ameliorates hyperglycemia-induced podocyte dysfunction.Podocyte-specific VEGF-a gain of function induces nodular glomerulosclerosis in eNOS null mice.Role of endothelial nitric oxide synthase in diabetic nephropathy: lessons from diabetic eNOS knockout mice Urinary excretion of fatty acid-binding protein 4 is associated with albuminuria and renal dysfunction.Reduced Krüppel-like factor 2 expression may aggravate the endothelial injury of diabetic nephropathy.Role of TRPM7 channels in hyperglycemia-mediated injury of vascular endothelial cells Endothelial dysfunction exacerbates renal interstitial fibrosis through enhancing fibroblast Smad3 linker phosphorylation in the mouse obstructed kidney.Glomerular endothelial cell injury and cross talk in diabetic kidney disease SDF-1/CXCR4 signaling preserves microvascular integrity and renal function in chronic kidney disease.Activation of nuclear factor erythroid 2-related factor 2 coordinates dimethylarginine dimethylaminohydrolase/PPAR-γ/endothelial nitric oxide synthase pathways that enhance nitric oxide generation in human glomerular endothelial cells.Arginase inhibition: a new treatment for preventing progression of established diabetic nephropathy Bone marrow derived myeloid cells orchestrate antiangiogenic resistance in glioblastoma through coordinated molecular networks.Comparison of Glomerular and Podocyte mRNA Profiles in Streptozotocin-Induced Diabetes.Activation of endothelial NAD(P)H oxidase accelerates early glomerular injury in diabetic mice Role of the eNOS-NO system in regulating the antiproteinuric effects of VEGF receptor 2 inhibition in diabetes.Endothelial-podocyte crosstalk: the missing link between endothelial dysfunction and albuminuria in diabetes.Anti-VEGFR2 driven nuclear translocation of VEGFR2 and acquired malignant hallmarks are mutation dependent in glioblastoma.Supplementation with Phycocyanobilin, Citrulline, Taurine, and Supranutritional Doses of Folic Acid and Biotin-Potential for Preventing or Slowing the Progression of Diabetic Complications.Role of Rho-GTPases and their regulatory proteins in glomerular podocyte function.Endothelial mitochondrial oxidative stress determines podocyte depletion in segmental glomerulosclerosis Exosomes from high glucose-treated glomerular endothelial cells trigger the epithelial-mesenchymal transition and dysfunction of podocytes Chimeric Mouse model to track the migration of bone marrow derived cells in glioblastoma following anti-angiogenic treatments.Pentraxin-3 Attenuates Renal Damage in Diabetic Nephropathy by Promoting M2 Macrophage Differentiation.Reduced Krüppel-Like Factor 2 Aggravates Glomerular Endothelial Cell Injury and Kidney Disease in Mice with Unilateral Nephrectomy.Chronic Hyperphosphatemia and Vascular Calcification Are Reduced by Stable Delivery of Soluble Klotho.Reduced muscarinic parotid secretion is underlain by impaired NO signaling in diabetic rabbits.Antiangiogenic Therapy for Diabetic Nephropathy.Reduced glomerular size selectivity in late streptozotocin-induced diabetes in rats: application of a distributed two-pore model.Antioxidant Role of Autophagy in Maintaining the Integrity of Glomerular Capillaries.Glomerular Endothelial Mitochondrial Dysfunction Is Essential and Characteristic of Diabetic Kidney Disease Susceptibility.Lysophosphatidic Acid Receptor Antagonism Protects against Diabetic Nephropathy in a Type 2 Diabetic Model.Cinacalcet-mediated activation of the CaMKKβ-LKB1-AMPK pathway attenuates diabetic nephropathy in db/db mice by modulation of apoptosis and autophagy.Nitric oxide production by glomerular podocytes.Janus Kinase 2 Regulates Transcription Factor EB Expression and Autophagy Completion in Glomerular Podocytes.Glomerular Endothelial Cells Stress and Cross-Talk With Podocytes in the Development of Diabetic Kidney Disease.

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eNOS deficiency predisposes podocytes to injury in diabetes.

http://www.wikidata.org/entity/Q36352132

description

2012 nî lūn-bûn

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2012年の論文

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2012年学术文章

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2012年学术文章

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2012年学术文章

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2012年学术文章

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2012年学术文章

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2012年學術文章

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2012年學術文章

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2012年學術文章

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name

eNOS deficiency predisposes podocytes to injury in diabetes.

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eNOS deficiency predisposes podocytes to injury in diabetes.

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type

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eNOS deficiency predisposes podocytes to injury in diabetes.

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eNOS deficiency predisposes podocytes to injury in diabetes.

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prefLabel

eNOS deficiency predisposes podocytes to injury in diabetes.

@ast

eNOS deficiency predisposes podocytes to injury in diabetes.

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Journal of the American Society of Nephrology

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eNOS deficiency predisposes podocytes to injury in diabetes

@en

P2093

Alison J Cox

http://www.w3.org/2001/XMLSchema#string

Andrew Advani

http://www.w3.org/2001/XMLSchema#string

Bailey E Stead

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Darren A Yuen

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Darren J Kelly

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Ian W Gibson

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Kathryn E White

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Kerri Thai

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Kim A Connelly

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Lei Zhu

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P2860

VEGF inhibition and renal thrombotic microangiopathy

Circulating microRNAs: biomarkers or mediators of cardiovascular diseases?

Fluorescent microangiography is a novel and widely applicable technique for delineating the renal microvasculature

Biochemistry and molecular cell biology of diabetic complications

PTK787/ZK 222584, a novel and potent inhibitor of vascular endothelial growth factor receptor tyrosine kinases, impairs vascular endothelial growth factor-induced responses and tumor growth after oral administration

Histone deacetylase inhibition attenuates diabetes-associated kidney growth: potential role for epigenetic modification of the epidermal growth factor receptor

Failure of blood-island formation and vasculogenesis in Flk-1-deficient mice

Heterozygous embryonic lethality induced by targeted inactivation of the VEGF gene

The pathobiology of diabetic complications: a unifying mechanism

eNOS knockout mice with advanced diabetic nephropathy have less benefit from renin-angiotensin blockade than from aldosterone receptor antagonists.

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1810-1823

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scholarly article

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10.1681/ASN.2011121170

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11

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23

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Takamune Takahashi

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2012-09-20T00:00:00Z

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22997257

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3482727

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