Chronic NOS inhibition actuates endothelial-mesenchymal transformation. - Wikidata - wikimedia - TriplyDB

Chronic NOS inhibition actuates endothelial-mesenchymal transformation.

Chronic NOS inhibition actuates endothelial-mesenchymal transformation.

http://www.wikidata.org/entity/Q50715902

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Angiogenesis inhibitor vasohibin-1 enhances stress resistance of endothelial cells via induction of SOD2 and SIRT1 The multifaceted role of the renal microvasculature during acute kidney injury Pathogenesis of endothelial cell dysfunction in chronic kidney disease: a retrospective and what the future may hold Acute Kidney Injury in Diabetes Mellitus The systemic nature of CKD.The Krebs cycle and mitochondrial mass are early victims of endothelial dysfunction: proteomic approach.Instructive Role of the Microenvironment in Preventing Renal Fibrosis Characterization of a model of an arteriovenous fistula in the rat: the effect of L-NAME Microvascular rarefaction: the decline and fall of blood vessels Fluorescence microangiography for quantitative assessment of peritubular capillary changes after AKI in mice Increased concentration of circulating angiogenesis and nitric oxide inhibitors induces endothelial to mesenchymal transition and myocardial fibrosis in patients with chronic kidney disease.D-4F, an apoA-1 mimetic, decreases airway hyperresponsiveness, inflammation, and oxidative stress in a murine model of asthma.Abnormal fibrillin-1 expression and chronic oxidative stress mediate endothelial mesenchymal transition in a murine model of systemic sclerosis.Impaired endothelial proliferation and mesenchymal transition contribute to vascular rarefaction following acute kidney injury.Glutamine supplementation alleviates vasculopathy and corrects metabolic profile in an in vivo model of endothelial cell dysfunction Curtailing endothelial TGF-β signaling is sufficient to reduce endothelial-mesenchymal transition and fibrosis in CKD Replicative aging induces endothelial to mesenchymal transition in human aortic endothelial cells: potential role of inflammation Elevated plasma levels of endostatin are associated with chronic kidney disease.Early Endothelial Progenitor Cells (eEPCs) in systemic sclerosis (SSc) - dynamics of cellular regeneration and mesenchymal transdifferentiation.Endostatin's emerging roles in angiogenesis, lymphangiogenesis, disease, and clinical applications.Endothelial Colony Forming Cells (ECFCs) in murine AKI - implications for future cell-based therapies.Number and function of peripheral blood endothelial progenitor cells in Henoch-Schönlein purpura nephritis children with different degrees of renal vascular lesions.Indolent course of tubulointerstitial disease in a mouse model of subpressor, low-dose nitric oxide synthase inhibition.Immune system in renal injury and repair: burning the candle from both ends?Mitochondria and reactive oxygen species.The role of cell plasticity in progression and reversal of renal fibrosis.Capillary rarefaction, hypoxia, VEGF and angiogenesis in chronic renal disease.Endothelium under stress: local and systemic messages.Fibrosis and heart failure.New insights in (inter)cellular mechanisms by heart failure with preserved ejection fraction.Endothelial progenitor cells: from senescence to rejuvenation.Hypoxia as a key player in the AKI-to-CKD transition.The third path of tubulointerstitial fibrosis: aberrant endothelial secretome.Postischemic microvasculopathy and endothelial progenitor cell-based therapy in ischemic AKI: update and perspectives.Stress-Induced Premature Senescence of Endothelial and Endothelial Progenitor Cells.Small Vessels, Big Role: Renal Microcirculation and Progression of Renal Injury.Endothelial colony-forming cells and pro-angiogenic cells: clarifying definitions and their potential role in mitigating acute kidney injury.Endothelial autophagy and Endothelial-to-Mesenchymal Transition (EndoMT) in eEPC treatment of ischemic AKI.Computational modeling of epithelial-mesenchymal transformations.Association of circulating angiogenesis inhibitors and asymmetric dimethyl arginine with coronary plaque burden.

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P2860

Chronic NOS inhibition actuates endothelial-mesenchymal transformation.

http://www.wikidata.org/entity/Q50715902

description

2006 nî lūn-bûn

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2006年の論文

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2006年学术文章

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2006年学术文章

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2006年学术文章

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2006年学术文章

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2006年学术文章

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2006年学术文章

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2006年學術文章

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2006年學術文章

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name

Chronic NOS inhibition actuates endothelial-mesenchymal transformation.

@en

Chronic NOS inhibition actuates endothelial-mesenchymal transformation.

@nl

type

label

Chronic NOS inhibition actuates endothelial-mesenchymal transformation.

@en

Chronic NOS inhibition actuates endothelial-mesenchymal transformation.

@nl

prefLabel

Chronic NOS inhibition actuates endothelial-mesenchymal transformation.

@en

Chronic NOS inhibition actuates endothelial-mesenchymal transformation.

@nl

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AJPHEART.00560.2006

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American Journal of Physiology - Heart and Circulatory Physiology

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Chronic NOS inhibition actuates endothelial-mesenchymal transformation.

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Daniel Patschan

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

Edmond O'Riordan

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

Jonathan Eskander

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

Leona Cohen-Gould

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Michael S Goligorsky

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Natalia Mendelev

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Praveen Chander

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Susann Patschan

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P2860

Epithelial-mesenchymal transition and its implications for fibrosis

Endostatin: an endogenous inhibitor of angiogenesis and tumor growth

Epithelial-mesenchymal transitions in development and pathologies

Evidence that fibroblasts derive from epithelium during tissue fibrosis

Advanced glycosylation products quench nitric oxide and mediate defective endothelium-dependent vasodilatation in experimental diabetes.

Endostatin's antiangiogenic signaling network.

In vivo bradykinin B2 receptor activation reduces renal fibrosis.

Remission of renal disease: recounting the challenge, acquiring the goal

Tubular epithelial-myofibroblast transdifferentiation mechanisms in proximal tubule cells.

Origin of interstitial fibroblasts in an accelerated model of angiotensin II-induced renal fibrosis.

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