The redox enzyme p66Shc contributes to diabetes and ischemia-induced delay in cutaneous wound healing. - Wikidata - wikimedia - TriplyDB

The redox enzyme p66Shc contributes to diabetes and ischemia-induced delay in cutaneous wound healing.

The redox enzyme p66Shc contributes to diabetes and ischemia-induced delay in cutaneous wound healing.

http://www.wikidata.org/entity/Q34082896

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The endothelium abridges insulin resistance to premature aging The Dual Function of Reactive Oxygen/Nitrogen Species in Bioenergetics and Cell Death: The Role of ATP Synthase Redox regulation of mitochondrial function Monoamine oxidases as sources of oxidants in the heart Deletion of p66Shc in mice increases the frequency of size-change mutations in the lacZ transgene Antioxidant sol-gel improves cutaneous wound healing in streptozotocin-induced diabetic rats.Endothelial properties of third-trimester amniotic fluid stem cells cultured in hypoxia Effects of cerium oxide nanoparticles on the growth of keratinocytes, fibroblasts and vascular endothelial cells in cutaneous wound healing.Soluble ST2 is regulated by p75 neurotrophin receptor and predicts mortality in diabetic patients with critical limb ischemia Recombinant adenovirus of human p66Shc inhibits MCF-7 cell proliferation.Endothelial progenitor cells in diabetes mellitus.p66Shc deletion or deficiency protects from obesity but not metabolic dysfunction in mice and humans.Protein tyrosine phosphatase 1B impairs diabetic wound healing through vascular endothelial growth factor receptor 2 dephosphorylation.Modelling the p53/p66Shc Aging Pathway in the Shortest Living Vertebrate Nothobranchius Furzeri.Redox Signaling in Diabetic Wound Healing Regulates Extracellular Matrix Deposition.Role of p66shc in skeletal muscle function.New aspects of p66Shc in ischaemia reperfusion injury and other cardiovascular diseases.Defective recruitment, survival and proliferation of bone marrow-derived progenitor cells at sites of delayed diabetic wound healing in mice.Targeting prolyl-isomerase Pin1 prevents mitochondrial oxidative stress and vascular dysfunction: insights in patients with diabetes.Blockade of PKCβ protects against remote organ injury induced by intestinal ischemia and reperfusion via a p66shc-mediated mitochondrial apoptotic pathway.p66Shc gene expression in peripheral blood mononuclear cells and progression of diabetic complications.The p66ShcA adaptor protein regulates healing after myocardial infarction.

P2860

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P2860

The redox enzyme p66Shc contributes to diabetes and ischemia-induced delay in cutaneous wound healing.

http://www.wikidata.org/entity/Q34082896

description

2010 nî lūn-bûn

@nan

2010 թուականի Յունիսին հրատարակուած գիտական յօդուած

@hyw

2010 թվականի հունիսին հրատարակված գիտական հոդված

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2010年の論文

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2010年論文

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2010年論文

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2010年論文

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2010年論文

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2010年論文

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2010年论文

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name

The redox enzyme p66Shc contri ...... ay in cutaneous wound healing.

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The redox enzyme p66Shc contri ...... ay in cutaneous wound healing.

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The redox enzyme p66Shc contri ...... ay in cutaneous wound healing.

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The redox enzyme p66Shc contri ...... ay in cutaneous wound healing.

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The redox enzyme p66Shc contri ...... ay in cutaneous wound healing.

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The redox enzyme p66Shc contri ...... ay in cutaneous wound healing.

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The redox enzyme p66Shc contri ...... ay in cutaneous wound healing.

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The redox enzyme p66Shc contri ...... ay in cutaneous wound healing.

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The redox enzyme p66Shc contri ...... ay in cutaneous wound healing.

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The redox enzyme p66Shc contri ...... lay in cutaneous wound healing

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P2093

Angelo Avogaro

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Annunziata Lapolla

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Chiara Cosma

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Elisa Boscaro

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Elisa Pagnin

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Elisabetta Iori

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Lisa Menegazzo

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Massimo Stendardo

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Pier Giuseppe Pelicci

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P2860

The p66shc adaptor protein controls oxidative stress response and life span in mammals

The pathobiology of diabetic complications: a unifying mechanism

Decreased superoxide production in macrophages of long-lived p66Shc knock-out mice.

Cutaneous wound healing: an update.

Diabetes and atherosclerosis: epidemiology, pathophysiology, and management.

Molecular pathogenesis of chronic wounds: the role of beta-catenin and c-myc in the inhibition of epithelialization and wound healing

Genetic deletion of p66(Shc) adaptor protein prevents hyperglycemia-induced endothelial dysfunction and oxidative stress.

Reducing the incidence of foot ulceration and amputation in diabetes.

The global burden of diabetic foot disease.

The molecular biology of chronic wounds and delayed healing in diabetes.

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2306-2314

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scholarly article

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10.2337/DB09-1727

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9

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59

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Gian Paolo Fadini

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2010-06-21T00:00:00Z

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44691136

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20566667

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2927954

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