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alpha1G-dependent T-type Ca2+ current antagonizes cardiac hypertrophy through a NOS3-dependent mechanism in mice

alpha1G-dependent T-type Ca2+ current antagonizes cardiac hypertrophy through a NOS3-dependent mechanism in mice

http://www.wikidata.org/entity/Q42690112

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Eps15 Homology Domain-containing Protein 3 Regulates Cardiac T-type Ca2+ Channel Targeting and Function in the Atria Cav3.2 T-type calcium channel is required for the NFAT-dependent Sox9 expression in tracheal cartilage Genetic deletion of the mitochondrial phosphate carrier desensitizes the mitochondrial permeability transition pore and causes cardiomyopathy Novel protective role of endogenous cardiac myocyte P2X4 receptors in heart failure Microdomain-specific localization of functional ion channels in cardiomyocytes: an emerging concept of local regulation and remodelling.TRPC channels are necessary mediators of pathologic cardiac hypertrophy.Electrophysiological remodeling in heart failure c-kit+ cells minimally contribute cardiomyocytes to the heart The IP3 receptor regulates cardiac hypertrophy in response to select stimuli.β-Adrenergic stimulation increases Cav3.1 activity in cardiac myocytes through protein kinase A Phorbol ester and endothelin-1 alter functional expression of Na+/Ca2+ exchange, K+, and Ca2+ currents in cultured neonatal rat myocytes T-type Ca²+ signalling regulates aldosterone-induced CREB activation and cell death through PP2A activation in neonatal cardiomyocytes Regulation and function of Cav3.1 T-type calcium channels in IGF-I-stimulated pulmonary artery smooth muscle cells.P2X4 receptor-eNOS signaling pathway in cardiac myocytes as a novel protective mechanism in heart failure.Genetic Analysis of Connective Tissue Growth Factor as an Effector of Transforming Growth Factor β Signaling and Cardiac Remodeling.The PTIP-Associated Histone Methyltransferase Complex Prevents Stress-Induced Maladaptive Cardiac Remodeling.Functional brown adipose tissue limits cardiomyocyte injury and adverse remodeling in catecholamine-induced cardiomyopathy.The Mitochondrial Calcium Uniporter Selectively Matches Metabolic Output to Acute Contractile Stress in the Heart Caveolin-3 Overexpression Attenuates Cardiac Hypertrophy via Inhibition of T-type Ca2+ Current Modulated by Protein Kinase Cα in Cardiomyocytes Tropomyosin dephosphorylation results in compensated cardiac hypertrophy Genetic lineage tracing identifies in situ Kit-expressing cardiomyocytes.Syndecan 4 signaling is required for exercise-induced cardiac hypertrophy.T-type Ca²⁺ channels regulate the exit of cardiac myocytes from the cell cycle after birth.Adenylyl cyclase 6 deletion increases mortality during sustained β-adrenergic receptor stimulation.CaMKII in the cardiovascular system: sensing redox states.Functional importance of T-type voltage-gated calcium channels in the cardiovascular and renal system: news from the world of knockout mice.Tetrodotoxin-sensitive Ca2+ Currents, but No T-type Currents in Normal, Hypertrophied, and Failing Mouse Cardiomyocytes.Cytokine Effects on Mechano-Induced Electrical Activity in Atrial Myocardium.T-type Ca2+ channels and autoregulation of local blood flow.Decreased cardiac L-type Ca²⁺ channel activity induces hypertrophy and heart failure in mice.Cardiac-directed expression of a catalytically inactive adenylyl cyclase 6 protects the heart from sustained β-adrenergic stimulation.Molecular pathways underlying cardiac remodeling during pathophysiological stimulation.Ca(2+) influx through L-type Ca(2+) channels and transient receptor potential channels activates pathological hypertrophy signaling A caveolae-targeted L-type Ca²+ channel antagonist inhibits hypertrophic signaling without reducing cardiac contractility.Calcium influx through Cav1.2 is a proximal signal for pathological cardiomyocyte hypertrophy.Early growth response 1 is an early signal inducing Cav3.2 T-type calcium channels during cardiac hypertrophy.TNF-α provokes electrical abnormalities in rat atrial myocardium via a NO-dependent mechanism.Evodiamine inhibits angiotensin II-induced rat cardiomyocyte hypertrophy.Increasing T-type calcium channel activity by β-adrenergic stimulation contributes to β-adrenergic regulation of heart rates.P/Q-type and T-type voltage-gated calcium channels are involved in the contraction of mammary and brain blood vessels from hypertensive patients.

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alpha1G-dependent T-type Ca2+ current antagonizes cardiac hypertrophy through a NOS3-dependent mechanism in mice

http://www.wikidata.org/entity/Q42690112

description

2009 nî lūn-bûn

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2009年论文

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2009年论文

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2009年论文

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name

alpha1G-dependent T-type Ca2+ ...... S3-dependent mechanism in mice

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alpha1G-dependent T-type Ca2+ ...... S3-dependent mechanism in mice

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type

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alpha1G-dependent T-type Ca2+ ...... S3-dependent mechanism in mice

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alpha1G-dependent T-type Ca2+ ...... S3-dependent mechanism in mice

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alpha1G-dependent T-type Ca2+ ...... S3-dependent mechanism in mice

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alpha1G-dependent T-type Ca2+ ...... S3-dependent mechanism in mice

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P2093

Arnold Schwartz

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Hiroyuki Nakayama

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Ilona Bodi

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Jeffrey Robbins

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John Lorenz

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Robert N Correll

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Steven R Houser

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P2860

Plasma membrane Ca2+-ATPase isoform 4 antagonizes cardiac hypertrophy in association with calcineurin inhibition in rodents

T-type calcium channel regulation by specific G-protein betagamma subunits

Canonical transient receptor potential channels promote cardiomyocyte hypertrophy through activation of calcineurin signaling

Caveolae and caveolins in the cardiovascular system

Stimulation of recombinant Ca(v)3.2, T-type, Ca(2+) channel currents by CaMKIIgamma(C)

Bradycardia and slowing of the atrioventricular conduction in mice lacking CaV3.1/alpha1G T-type calcium channels

Localization of cardiac L-type Ca(2+) channels to a caveolar macromolecular signaling complex is required for beta(2)-adrenergic regulation

PKC-alpha regulates cardiac contractility and propensity toward heart failure

Reexpression of T-type Ca2+ channel gene and current in post-infarction remodeled rat left ventricle.

Concentric left ventricular remodeling in endothelial nitric oxide synthase knockout mice by chronic pressure overload.

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3787-3796

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10.1172/JCI39724

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12

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119

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Jeffery D. Molkentin

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2009-11-16T00:00:00Z

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38096152

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19920353

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2786799

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