Blockade of endothelial-mesenchymal transition by a Smad3 inhibitor delays the early development of streptozotocin-induced diabetic nephropathy - Wikidata - awgldk - TriplyDB

Blockade of endothelial-mesenchymal transition by a Smad3 inhibitor delays the early development of streptozotocin-induced diabetic nephropathy

Blockade of endothelial-mesenchymal transition by a Smad3 inhibitor delays the early development of streptozotocin-induced diabetic nephropathy

http://www.wikidata.org/entity/Q35757154

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Endothelial-Mesenchymal Transition in Regenerative Medicine Epithelial-to-Mesenchymal Transition in Diabetic Nephropathy: Fact or Fiction?TGF-β/Smad signaling in renal fibrosis Regulation of endothelial cell plasticity by TGF-β Smads as therapeutic targets for chronic kidney disease Excessive vascular sprouting underlies cerebral hemorrhage in mice lacking αVβ8-TGFβ signaling in the brain.Role of the TGF-β/BMP-7/Smad pathways in renal diseases Cellular mechanisms of tissue fibrosis. 1. Common and organ-specific mechanisms associated with tissue fibrosis.Controlling the receptor for advanced glycation end-products to conquer diabetic vascular complications Redox control of p53 in the transcriptional regulation of TGF-β1 target genes through SMAD cooperativity.Glomerular endothelial cell injury and damage precedes that of podocytes in adriamycin-induced nephropathy.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 Knockout of toll-like receptor-2 attenuates both the proinflammatory state of diabetes and incipient diabetic nephropathy Role of endothelial-mesenchymal transition (EndoMT) in the pathogenesis of fibrotic disorders Regulation of RAGE for attenuating progression of diabetic vascular complications.The inflammatory response in myocardial injury, repair, and remodelling.BAMBI elimination enhances alternative TGF-β signaling and glomerular dysfunction in diabetic mice Glucagon-Like Peptide 1 Protects against Hyperglycemic-Induced Endothelial-to-Mesenchymal Transition and Improves Myocardial Dysfunction by Suppressing Poly(ADP-Ribose) Polymerase 1 Activity.Transforming growth factor beta signaling in adult cardiovascular diseases and repair.GQ5 Hinders Renal Fibrosis in Obstructive Nephropathy by Selectively Inhibiting TGF-β-Induced Smad3 Phosphorylation Cellular and molecular mechanisms of renal fibrosis.Renal interstitial fibrosis: mechanisms and evaluation.Netrin-1 attenuates the progression of renal dysfunction by blocking endothelial-to-mesenchymal transition in the 5/6 nephrectomy rat model.Increased urinary Smad3 is significantly correlated with glomerular hyperfiltration and a reduced glomerular filtration rate and is a new urinary biomarker for diabetic nephropathy.Endothelial-mesenchymal transition and its contribution to the emergence of stem cell phenotype Epithelial-mesenchymal transition and mesenchymal-epithelial transition response during differentiation of growth-plate chondrocytes in endochondral ossification Store-Operated Ca2+ Channels in Mesangial Cells Inhibit Matrix Protein Expression.P311 promotes renal fibrosis via TGFβ1/Smad signaling.High glucose mediates endothelial-to-chondrocyte transition in human aortic endothelial cells.Treatment of renal fibrosis by rebalancing TGF-β/Smad signaling with the combination of asiatic acid and naringenin.Role of Transforming Growth Factor-β1 and Smads Signaling Pathway in Intrauterine Adhesion.Quercetin Inhibits Fibroblast Activation and Kidney Fibrosis Involving the Suppression of Mammalian Target of Rapamycin and β-catenin Signaling.In Pulmonary Arterial Hypertension, Reduced BMPR2 Promotes Endothelial-to-Mesenchymal Transition via HMGA1 and Its Target Slug TGF-β/Smad3 signalling regulates the transition of bone marrow-derived macrophages into myofibroblasts during tissue fibrosis Yap1 promotes the survival and self-renewal of breast tumor initiating cells via inhibiting Smad3 signaling Cytokine mediated tissue fibrosis Bleomycin induces endothelial mesenchymal transition through activation of mTOR pathway: a possible mechanism contributing to the sclerotherapy of venous malformations.Diverse roles of TGF-β/Smads in renal fibrosis and inflammation.Role of TGF-β in chronic kidney disease: an integration of tubular, glomerular and vascular effects.

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P2860

Blockade of endothelial-mesenchymal transition by a Smad3 inhibitor delays the early development of streptozotocin-induced diabetic nephropathy

http://www.wikidata.org/entity/Q35757154

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2010年论文

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2010年论文

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Blockade of endothelial-mesenc ...... n-induced diabetic nephropathy

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Blockade of endothelial-mesenc ...... n-induced diabetic nephropathy

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Blockade of endothelial-mesenc ...... n-induced diabetic nephropathy

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Blockade of endothelial-mesenc ...... n-induced diabetic nephropathy

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Georgina Caruana

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Hiroshi Yamamoto

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Jun Yao

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Xinli Qu

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Yasuhiko Yamamoto

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P2860

Receptor for advanced glycation end products (RAGE)-mediated neurite outgrowth and activation of NF-kappaB require the cytoplasmic domain of the receptor but different downstream signaling pathways

Renoprotective effect of the angiotensin-receptor antagonist irbesartan in patients with nephropathy due to type 2 diabetes

Oxidative stress as a major culprit in kidney disease in diabetes

Advanced glycation end products cause epithelial-myofibroblast transdifferentiation via the receptor for advanced glycation end products (RAGE)

Effects of losartan on renal and cardiovascular outcomes in patients with type 2 diabetes and nephropathy

Endothelial-to-mesenchymal transition contributes to cardiac fibrosis

PKC-beta1 mediates glucose-induced Akt activation and TGF-beta1 upregulation in mesangial cells.

RAGE: a new target for the prevention and treatment of the vascular and inflammatory complications of diabetes.

Renal and retinal effects of enalapril and losartan in type 1 diabetes

Receptor for advanced glycation endproducts (RAGE) and the complications of diabetes.

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45494041

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