Flow (shear stress)-induced endothelium-dependent dilation is altered in mice lacking the gene encoding for dystrophin
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Impaired flow-induced dilation in mesenteric resistance arteries from receptor protein tyrosine phosphatase-mu-deficient miceInvolvement of angiotensin II in the remodeling induced by a chronic decrease in blood flow in rat mesenteric resistance arteriesKey role of alpha(1)beta(1)-integrin in the activation of PI3-kinase-Akt by flow (shear stress) in resistance arteriesNotch3 is a major regulator of vascular tone in cerebral and tail resistance arteriesStimulation of angiotensin AT2 receptors by the non-peptide agonist, Compound 21, evokes vasodepressor effects in conscious spontaneously hypertensive rats.Vasodilation of intramuscular arterioles under shear stress in dystrophin-deficient skeletal muscle is impaired through decreased nNOS expression.Membrane sealant Poloxamer P188 protects against isoproterenol induced cardiomyopathy in dystrophin deficient mice.Preclinical drug trials in the mdx mouse: assessment of reliable and sensitive outcome measures.Increased neointimal thickening in dystrophin-deficient mdx mice.Vascular TRP channels: performing under pressure and going with the flowEvidence for impaired neurovascular transmission in a murine model of Duchenne muscular dystrophy.Long Lasting Microvascular Tone Alteration in Rat Offspring Exposed In Utero to Maternal Hyperglycaemia.Dystrophin deficiency reduces atherosclerotic plaque development in ApoE-null miceEffect of Periodic Granulocyte Colony-Stimulating Factor Administration on Endothelial Progenitor Cells and Different Monocyte Subsets in Pediatric Patients with Muscular Dystrophies.Dystrophin-deficient cardiomyopathy in mouse: expression of Nox4 and Lox are associated with fibrosis and altered functional parameters in the heartThe shear stress of it all: the cell membrane and mechanochemical transductionProgress in gene therapy of dystrophic heart disease.Notch transcriptional control of vascular smooth muscle regulatory gene expression and function.Vascular-targeted therapies for Duchenne muscular dystrophyInjection of vessel-derived stem cells prevents dilated cardiomyopathy and promotes angiogenesis and endogenous cardiac stem cell proliferation in mdx/utrn-/- but not aged mdx mouse models for duchenne muscular dystrophy.Hypoxia-induced cardiac injury in dystrophic mice.Role of the cytoskeleton in flow (shear stress)-induced dilation and remodeling in resistance arteries.A new trick for an old dogma: ENaC proteins as mechanotransducers in vascular smooth muscle.Coronary adventitial cells are linked to perivascular cardiac fibrosis via TGFβ1 signaling in the mdx mouse model of Duchenne muscular dystrophy.Membrane Injury and Repair in the Muscular Dystrophies.Skeletal Muscle Microvasculature: A Highly Dynamic Lifeline.Omega-3 Polyunsaturated Fatty Acids Protect Against Cigarette Smoke-Induced Oxidative Stress and Vascular Dysfunction.Increased plasma lipid levels exacerbate muscle pathology in the mdx mouse model of Duchenne muscular dystrophyImpaired vascular mechanotransduction in a transgenic mouse model of CADASIL arteriopathy.Quantification of the mechanical behavior of carotid arteries from wild-type, dystrophin-deficient, and sarcoglycan-delta knockout mice.Implications for Cardiac Function Following Rescue of the Dystrophic Diaphragm in a Mouse Model of Duchenne Muscular Dystrophy.Absence of dystrophin in mice reduces NO-dependent vascular function and vascular density: total recovery after a treatment with the aminoglycoside gentamicin.Flt-1 haploinsufficiency ameliorates muscular dystrophy phenotype by developmentally increased vasculature in mdx mice.Mechanics of carotid arteries in a mouse model of Marfan Syndrome.Multipotential mesoangioblast stem cell therapy in the mdx/utrn-/- mouse model for Duchenne muscular dystrophy.Altered biomechanical properties of carotid arteries in two mouse models of muscular dystrophy.Early hypercholesterolemia contributes to vasomotor dysfunction and injury associated atherogenesis that can be inhibited by nitric oxide.Type 2 diabetes severely impairs structural and functional adaptation of rat resistance arteries to chronic changes in blood flow.Deletion of MLCK210 induces subtle changes in vascular reactivity but does not affect cardiac function.A deficit of brain dystrophin 71 impairs hypothalamic osmostat.
P2860
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P2860
Flow (shear stress)-induced endothelium-dependent dilation is altered in mice lacking the gene encoding for dystrophin
description
2001 nî lūn-bûn
@nan
2001 թուականի Փետրուարին հրատարակուած գիտական յօդուած
@hyw
2001 թվականի փետրվարին հրատարակված գիտական հոդված
@hy
2001年の論文
@ja
2001年論文
@yue
2001年論文
@zh-hant
2001年論文
@zh-hk
2001年論文
@zh-mo
2001年論文
@zh-tw
2001年论文
@wuu
name
Flow (shear stress)-induced en ...... e gene encoding for dystrophin
@ast
Flow (shear stress)-induced en ...... e gene encoding for dystrophin
@en
Flow (shear stress)-induced en ...... e gene encoding for dystrophin
@nl
type
label
Flow (shear stress)-induced en ...... e gene encoding for dystrophin
@ast
Flow (shear stress)-induced en ...... e gene encoding for dystrophin
@en
Flow (shear stress)-induced en ...... e gene encoding for dystrophin
@nl
prefLabel
Flow (shear stress)-induced en ...... e gene encoding for dystrophin
@ast
Flow (shear stress)-induced en ...... e gene encoding for dystrophin
@en
Flow (shear stress)-induced en ...... e gene encoding for dystrophin
@nl
P2093
P2860
P356
P1433
P1476
Flow (shear stress)-induced en ...... e gene encoding for dystrophin
@en
P2093
K Matrougui
L Loufrani
P2860
P304
P356
10.1161/01.CIR.103.6.864
P407
P577
2001-02-13T00:00:00Z