Acute Rho-kinase inhibition improves coronary dysfunction in vivo, in the early diabetic microcirculation
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Contractile apparatus dysfunction early in the pathophysiology of diabetic cardiomyopathyCaffeic acid phenethyl amide ameliorates ischemia/reperfusion injury and cardiac dysfunction in streptozotocin-induced diabetic rats.Endothelial progenitor cells transplantation attenuated blood-brain barrier damage after ischemia in diabetic mice via HIF-1α.Treadmill running improves hindlimb arteriolar endothelial function in type 1 diabetic mice as visualized by X-ray microangiographyChronic Rho-kinase inhibition improves left ventricular contractile dysfunction in early type-1 diabetes by increasing myosin cross-bridge extension.Involvement of Rho-associated protein kinase (ROCK) and bone morphogenetic protein-binding endothelial cell precursor-derived regulator (BMPER) in high glucose-increased alkaline phosphatase expression and activity in human coronary artery smooth muRhoA/rock signaling mediates peroxynitrite-induced functional impairment of Rat coronary vesselsThe soluble guanylate cyclase activator cinaciguat prevents cardiac dysfunction in a rat model of type-1 diabetes mellitusPlakophilin-2 loss promotes TGF-β1/p38 MAPK-dependent fibrotic gene expression in cardiomyocytes.Interdisciplinary approach to compensation of hypoglycemia in diabetic patients with chronic heart failure.Vessel Dilation Attenuates Endothelial Dysfunction Following Middle Cerebral Artery Occlusion in Hyperglycemic Rats.Analysis of the microvascular morphology and hemodynamics of breast cancer in mice using SPring-8 synchrotron radiation microangiographyTissue-engineered smooth muscle cell and endothelial progenitor cell bi-level cell sheets prevent progression of cardiac dysfunction, microvascular dysfunction, and interstitial fibrosis in a rodent model of type 1 diabetes-induced cardiomyopathy.Inhibition of Rho kinase protects from ischaemia-reperfusion injury via regulation of arginase activity and nitric oxide synthase in type 1 diabetes.The Rho kinase inhibitor, fasudil, ameliorates diabetes-induced cardiac dysfunction by improving calcium clearance and actin remodeling.Progressive Decrease in Coronary Vascular Function Associated With Type 2 Diabetic Heart Disease.
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P2860
Acute Rho-kinase inhibition improves coronary dysfunction in vivo, in the early diabetic microcirculation
description
article científic
@ca
article scientifique
@fr
articolo scientifico
@it
artigo científico
@pt
bilimsel makale
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scientific article published on August 2013
@en
vedecký článok
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vetenskaplig artikel
@sv
videnskabelig artikel
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vědecký článek
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name
Acute Rho-kinase inhibition im ...... arly diabetic microcirculation
@en
Acute Rho-kinase inhibition im ...... rly diabetic microcirculation.
@nl
type
label
Acute Rho-kinase inhibition im ...... arly diabetic microcirculation
@en
Acute Rho-kinase inhibition im ...... rly diabetic microcirculation.
@nl
prefLabel
Acute Rho-kinase inhibition im ...... arly diabetic microcirculation
@en
Acute Rho-kinase inhibition im ...... rly diabetic microcirculation.
@nl
P2093
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P356
P1476
Acute Rho-kinase inhibition im ...... arly diabetic microcirculation
@en
P2093
Amanda J Edgley
Darren J Kelly
Daryl O Schwenke
Hirotsugu Tsuchimochi
Keiji Umetani
Mandar Joshi
Mark T Waddingham
Mathew J Jenkins
Mikiyasu Shirai
Misa Yoshimoto
P2860
P2888
P356
10.1186/1475-2840-12-111
P407
P577
2013-08-01T00:00:00Z
P5875
P6179
1030655589