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Dysregulation of HSG triggers vascular proliferative disorders
Vascular proliferative disorders, such as atherosclerosis and restenosis, are the most common causes of severe cardiovascular diseases, but a common molecular mechanism remains elusive. Here, weExpand
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CaMKII is a RIP3 substrate mediating ischemia- and oxidative stress–induced myocardial necroptosis
Regulated necrosis (necroptosis) and apoptosis are crucially involved in severe cardiac pathological conditions, including myocardial infarction, ischemia-reperfusion injury and heart failure.Expand
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ASF/SF2-Regulated CaMKIIδ Alternative Splicing Temporally Reprograms Excitation-Contraction Coupling in Cardiac Muscle
The transition from juvenile to adult life is accompanied by programmed remodeling in many tissues and organs, which is key for organisms to adapt to the demand of the environment. Here we report aExpand
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High Basal Protein Kinase A–Dependent Phosphorylation Drives Rhythmic Internal Ca2+ Store Oscillations and Spontaneous Beating of Cardiac Pacemaker Cells
Local, rhythmic, subsarcolemmal Ca2+ releases (LCRs) from the sarcoplasmic reticulum (SR) during diastolic depolarization in sinoatrial nodal cells (SANC) occur even in the basal state and activateExpand
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Linkage of beta1-adrenergic stimulation to apoptotic heart cell death through protein kinase A-independent activation of Ca2+/calmodulin kinase II.
beta(1)-adrenergic receptor (beta(1)AR) stimulation activates the classic cAMP/protein kinase A (PKA) pathway to regulate vital cellular processes from the change of gene expression to the control ofExpand
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Central role of E3 ubiquitin ligase MG53 in insulin resistance and metabolic disorders
Insulin resistance is a fundamental pathogenic factor present in various metabolic disorders including obesity and type 2 diabetes. Although skeletal muscle accounts for 70–90% of insulin-stimulatedExpand
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Dilated cardiomyopathy caused by tissue‐specific ablation of SC35 in the heart
Many genetic diseases are caused by mutations in cis‐acting splicing signals, but few are triggered by defective trans‐acting splicing factors. Here we report that tissue‐specific ablation of theExpand
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The β2-Adrenergic receptor delivers an antiapoptotic signal to cardiac myocytes through Gi-Dependent coupling to phosphatidylinositol 3'-kinase
Abstract—Recent studies have shown that chronic β-adrenergic receptor (β-AR) stimulation alters cardiac myocyte survival in a receptor subtype-specific manner. We examined the effect of selective β1-Expand
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Sustained beta1-adrenergic stimulation modulates cardiac contractility by Ca2+/calmodulin kinase signaling pathway.
A tenet of beta1-adrenergic receptor (beta1AR) signaling is that stimulation of the receptor activates the adenylate cyclase-cAMP-protein kinase A (PKA) pathway, resulting in positive inotropic andExpand
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Mitofusin-2 Is a Major Determinant of Oxidative Stress-mediated Heart Muscle Cell Apoptosis*
An inexorable loss of terminally differentiated heart muscle cells is a crucial causal factor for heart failure. Here, we have provided several lines of evidence to demonstrate that mitofusin-2Expand
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