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Suppressors of cytokine signaling abrogate diabetic nephropathy.

Suppressors of cytokine signaling abrogate diabetic nephropathy.

http://www.wikidata.org/entity/Q39735007

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Horizon 2020 in Diabetic Kidney Disease: The Clinical Trial Pipeline for Add-On Therapies on Top of Renin Angiotensin System Blockade The role of the Janus kinase family/signal transducer and activator of transcription signaling pathway in fibrotic renal disease Present and future in the treatment of diabetic kidney disease Diabetic Kidney Disease: Pathophysiology and Therapeutic Targets 2017 update on the relationship between diabetes and colorectal cancer: epidemiology, potential molecular mechanisms and therapeutic implications Discovering hidden relationships between renal diseases and regulated genes through 3D network visualizations.SOCS3 overexpression inhibits advanced glycation end product-induced EMT in proximal tubule epithelial cells DJC Suppresses Advanced Glycation End Products-Induced JAK-STAT Signaling and ROS in Mesangial Cells Role of transcription factor acetylation in diabetic kidney disease.IL-18 induces profibrotic renal tubular cell injury via STAT3 activation.The cleaved cytoplasmic tail of polycystin-1 regulates Src-dependent STAT3 activation.Inflammation in diabetic kidney disease Effects of 1,25-(OH)(2)D (3) on the expressions of vitamin D receptor, STAT5 and cytoskeletal rearrangement in human monocytes incubated with sera from type 2 diabetes patients and diabetic nephropathy patients with uremia.New targets for treatment of diabetic nephropathy: what we have learned from animal models.Decorin, erythroblastic leukaemia viral oncogene homologue B4 and signal transducer and activator of transcription 3 regulation of semaphorin 3A in central nervous system scar tissue Anti-inflammatory effect of 1,25-dihydroxyvitamin D3 is associated with crosstalk between signal transducer and activator of transcription 5 and the vitamin D receptor in human monocytes Absence of nicotinic acetylcholine receptor α7 subunit amplifies inflammation and accelerates onset of fibrosis: an inflammatory kidney model.Interferon-γ biphasically regulates angiotensinogen expression via a JAK-STAT pathway and suppressor of cytokine signaling 1 (SOCS1) in renal proximal tubular cells.Identification of cross-species shared transcriptional networks of diabetic nephropathy in human and mouse glomeruli.Adipose-Derived Mesenchymal Stem Cells Transplantation Alleviates Renal Injury in Streptozotocin-Induced Diabetic Nephropathy Transcriptional networks of murine diabetic peripheral neuropathy and nephropathy: common and distinct gene expression patterns.JAK-STAT and the renin-angiotensin system: The role of the JAK-STAT pathway in blood pressure and intrarenal renin-angiotensin system regulation Treatment of diabetic nephropathy with Tripterygium wilfordii Hook F extract: a prospective, randomized, controlled clinical trial miR-150 promotes renal fibrosis in lupus nephritis by downregulating SOCS1 Protective effects of miR-29a on diabetic glomerular dysfunction by modulation of DKK1/Wnt/β-catenin signaling Macrophage-derived IL-6 contributes to ANG II-mediated angiotensinogen stimulation in renal proximal tubular cells.Renal function in diabetic disease models: the tubular system in the pathophysiology of the diabetic kidney.Therapeutic effects of suppressors of cytokine signaling in diabetic nephropathy.Activation of PI3K in response to high glucose leads to regulation of SOCS-3 and STAT1/3 signals and induction of glomerular mesangial extracellular matrix formation.Antifibrotic treatment and other new strategies for improving renal outcomes Targeting inflammation in cardiovascular diseases. still a neglected field?Chromatin modifications associated with diabetes.SOCS and diabetes--ups and downs of a turbulent relationship.Therapeutic approaches to diabetic nephropathy--beyond the RAS.JAK inhibition and progressive kidney disease.Key pathways in renal disease progression of experimental diabetes.Therapies on the Horizon for Diabetic Kidney Disease.Targeting inflammation in diabetic kidney disease: early clinical trials.Fluorofenidone protects against renal fibrosis by inhibiting STAT3 tyrosine phosphorylation.JAK inhibition in the treatment of diabetic kidney disease.

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P2860

Suppressors of cytokine signaling abrogate diabetic nephropathy.

http://www.wikidata.org/entity/Q39735007

description

2010 nî lūn-bûn

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2010年の論文

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2010年学术文章

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2010年学术文章

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2010年学术文章

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2010年学术文章

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2010年学术文章

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2010年學術文章

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2010年學術文章

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2010年學術文章

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name

Suppressors of cytokine signaling abrogate diabetic nephropathy.

@en

Suppressors of cytokine signaling abrogate diabetic nephropathy.

@nl

type

label

Suppressors of cytokine signaling abrogate diabetic nephropathy.

@en

Suppressors of cytokine signaling abrogate diabetic nephropathy.

@nl

prefLabel

Suppressors of cytokine signaling abrogate diabetic nephropathy.

@en

Suppressors of cytokine signaling abrogate diabetic nephropathy.

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P1433

Journal of the American Society of Nephrology

P1476

Suppressors of cytokine signaling abrogate diabetic nephropathy.

@en

P2093

Ana Sanz

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

Beñat Mallavia

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

Carmen Gomez-Guerrero

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Claudio Flores

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Guadalupe Ortiz-Muñoz

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Jesus Egido

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Julia Blanco

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Oscar Lopez-Franco

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Sergio Mezzano

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Virginia Lopez-Parra

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P2860

From hyperglycemia to diabetic kidney disease: the role of metabolic, hemodynamic, intracellular factors and growth factors/cytokines

Induction of the cytokine signal regulator SOCS3/CIS3 as a therapeutic strategy for treating inflammatory arthritis

Fluvastatin inhibits activation of JAK and STAT proteins in diabetic rat glomeruli and mesangial cells under high glucose conditions

Inflammatory mechanisms of diabetic complications.

Role of high glucose-induced nuclear factor-kappaB activation in monocyte chemoattractant protein-1 expression by mesangial cells.

SOCS-3 negatively regulates innate and adaptive immune mechanisms in acute IL-1-dependent inflammatory arthritis.

Suppressor of cytokine signaling-1 regulates acute inflammatory arthritis and T cell activation.

Mechanisms of tubulointerstitial injury in the kidney: final common pathways to end-stage renal failure.

Controlling cytokine signaling by constitutive inhibitors.

STAT1 as a new molecular target of anti-inflammatory treatment.

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763-772

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scholarly article

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10.1681/ASN.2009060625

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5

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21

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Paula Fernandez-Vizarra

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2010-02-25T00:00:00Z

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41578339

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20185635

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2865742

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