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heart failure/phosphatase
Nuoroda įrašoma į mainų sritį
Puslapis 1 nuo 524 rezultatus
Differential regulation of protein phosphatase 1 (PP1) isoforms in human heart failure and atrial fibrillation.
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Protein phosphatase 1 (PP1) is a key regulator of important cardiac signaling pathways. Dysregulation of PP1 has been heavily implicated in cardiac dysfunctions. Accordingly, pharmacological targeting of PP1 activity is considered for therapeutic intervention in human cardiomyopathies. Recent
Inhibition of protein phosphatase 1 by inhibitor-2 gene delivery ameliorates heart failure progression in genetic cardiomyopathy.
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The type 1 protein phosphatase (PP1) has been reported to be overactivated in the failing heart, leading to a depression in cardiac function. We investigated whether in vivo PP1 inhibition by myocardial gene transfer of inhibitor-2 (INH-2), an endogenous PP1 inhibitor, alleviates heart failure (HF)
Heart failure-inducible gene therapy targeting protein phosphatase 1 prevents progressive left ventricular remodeling.
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BACKGROUND
The targeting of Ca(2+) cycling has emerged as a potential therapy for the treatment of severe heart failure. These approaches include gene therapy directed at overexpressing sarcoplasmic reticulum (SR) Ca(2+) ATPase, or ablation of phospholamban (PLN) and associated protein phosphatase 1
Astragalosides increase the cardiac diastolic function and regulate the "Calcium sensing receptor-protein kinase C-protein phosphatase 1" pathway in rats with heart failure.
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This study was designed to investigate the effects of astragalosides on cardiac diastolic function, and an emphasis was placed on the variation of the upstream molecular regulators of phospholamban. Chronic heart failure (CHF) rats were induced by ligaturing the left anterior coronary artery, and
Differential gene expression in skeletal muscle after induction of heart failure: impact of cytokines on protein phosphatase 2A expression.
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Different intrinsic alterations of skeletal muscle metabolism and gene expression have been described in chronic heart failure (CHF). As proposed skeletal muscle alterations in CHF may contribute to exercise intolerance and early muscular fatigue. However the exact molecular changes occurring in the
Chronic receptor-mediated activation of Gi/o proteins alters basal t-tubular and sarcolemmal L-type Ca²⁺ channel activity through phosphatases in heart failure.
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L-type Ca(2+) channels (LTCCs) play an essential role in the excitation-contraction coupling of ventricular myocytes. We previously found that t-tubular (TT) LTCC current density was halved by the activation of protein phosphatase (PP)1 and/or PP2A, whereas surface sarcolemmal (SS) LTCC current
Connexin 43 downregulation and dephosphorylation in nonischemic heart failure is associated with enhanced colocalized protein phosphatase type 2A.
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In nonischemic heart failure (HF), ventricular tachycardia initiates by a nonreentrant mechanism, but there is altered conduction (that could lead to re-entry) that could arise from changes in gap junctional proteins, especially connexin43 (Cx43). We studied Cx43 expression and phosphorylation state
Improvement of peripheral endothelial dysfunction by protein tyrosine phosphatase inhibitors in heart failure.
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BACKGROUND
Chronic heart failure (CHF) induces endothelial dysfunction characterized by a decrease in nitric oxide (NO) production in response to flow (flow-mediated dilatation [FMD]). Because activation of endothelial NO synthase (eNOS) by flow requires tyrosine phosphorylation, we tested whether
[Effects of valsartan on sarcoplasmic reticulum calcium adenosine triphosphatase, protein kinase A and protein phosphatase 1 alpha in a rabbit model of heart failure].
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OBJECTIVE
To investigate the effects of valsartan on expressions of myocardial sarcoplasmic reticulum calcium adenosine triphosphatase (SERCA2), protein kinase A (PKA) and protein phosphatase 1 alpha (PP1alpha) in a rabbit model of heart failure.
METHODS
Rabbits were divided into sham-operated
Rearrangement of the Protein Phosphatase 1 Interactome During Heart Failure Progression.
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BACKGROUND
Heart failure (HF) is a complex disease with a rising prevalence despite advances in treatment. Protein phosphatase 1 (PP1) has long been implicated in HF pathogenesis, but its exact role is both unclear and controversial. Most previous studies measured only the PP1 catalytic subunit
Vascular reactivity in heart failure: role of myosin light chain phosphatase.
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Congestive heart failure (CHF) is a clinical syndrome, which is the result of systolic or diastolic ventricular dysfunction. During CHF, vascular tone is regulated by the interplay of neurohormonal mechanisms and endothelial-dependent factors and is characterized by both central and peripheral
The potential role of MLC phosphatase and MAPK signalling in the pathogenesis of vascular dysfunction in heart failure.
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The clinical syndrome of heart failure is associated with both a resting vasoconstriction and reduced sensitivity to nitric oxide mediated vasodilatation, and this review will focus on the role of myosin light chain (MLC) phosphatase in the pathogenesis of the vascular abnormalities of heart
Serum alkaline phosphatase as a predictor of worsening renal function in patients with acute decompensated heart failure.
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BACKGROUND
Venous congestion has come into focus as an important hemodynamic factor for worsening renal function (WRF) in patients with acute decompensated heart failure (ADHF). Serum alkaline phosphatase (ALP) was reported as a biological marker of liver congestion in ADHF. The purpose of this
Altered phosphatase activity in heart failure, influence on Ca2+ movement.
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Many cardiac proteins undergo reversible phosphorylation. While the protein kinases which bring about phosphorylations are well studied, less effort has been put into the dephosphorylating phosphatases (for an earlier review compare 14). An important event in the heart, which is controlled by
The human G147D-protein phosphatase 1 inhibitor-1 polymorphism is not associated with altered clinical characteristics in heart failure.
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OBJECTIVE
A human protein phosphatase inhibitor-1 polymorphism, G147D (c.440G>A, p.147G>D), has been previously demonstrated to blunt the contractile responses of cardiomyocytes to beta-adrenergic agonists. The present study sought to examine whether the G147D inhibitor-1 polymorphism may be
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