Journal ArticleDOI
Pressure- and Volume-Induced Left Ventricular Hypertrophies Are Associated With Distinct Myocyte Phenotypes and Differential Induction of Peptide Growth Factor mRNAs
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TLDR
Stimulus-specific heterogeneity in the signaling events and peptide growth factors coupled to gene expression could play a role in determining the type of hypertrophy that is caused by various forms of hemodynamic overload.Abstract:
Background Chronic pressure and volume overload (PO and VO) result in morphologically and functionally distinct forms of myocardial hypertrophy. We tested the hypothesis that PO- and VO-induced lef...read more
Citations
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Journal ArticleDOI
Hypertrophy of the heart: a new therapeutic target?
TL;DR: Observations from animal models and clinical trials that suggest benefit from an antihypertrophic strategy are summarized and signaling pathways that hold promise as potential targets for therapeutic intervention are focused on.
Journal ArticleDOI
Norepinephrine Stimulates Apoptosis in Adult Rat Ventricular Myocytes by Activation of the β-Adrenergic Pathway
TL;DR: NE, acting via the ss-adrenergic pathway, stimulates apoptosis in adult rat cardiac myocytes in vitro and requires calcium entry via voltage-dependent calcium channels, which may contribute to the progression of myocardial failure.
Journal ArticleDOI
Myocardial structure and function differ in systolic and diastolic heart failure.
Loek van Heerebeek,Attila Borbély,Hans W.M. Niessen,Jean G.F. Bronzwaer,Jolanda van der Velden,Ger J.M. Stienen,Wolfgang A. Linke,Gerrit J Laarman,Walter Paulus +8 more
TL;DR: LV myocardial structure and function differ in SHF and DHF because of distinct cardiomyocyte abnormalities, and these findings support the clinical separation of heart failure patients into SHF or DHF phenotypes.
Journal ArticleDOI
Mechanical stress-induced cardiac hypertrophy: mechanisms and signal transduction pathways.
C. Ruwhof,A. van der Laarse +1 more
TL;DR: The primary effects of mechanical stress are focused on: how mechanical stress may be sensed, and which signal transduction pathways may couple mechanical stress to modulation of gene expression, and to increased protein synthesis.
Journal ArticleDOI
Nitric oxide, atrial natriuretic peptide, and cyclic GMP inhibit the growth-promoting effects of norepinephrine in cardiac myocytes and fibroblasts.
TL;DR: It is indicated that nitric oxide and ANP can attenuate the effects of NE on the growth of cardiac myocytes and fibroblasts, most likely by a cGMP-mediated inhibition of NE-stimulated Ca2+ influx.
References
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Journal ArticleDOI
Single-step method of RNA isolation by acid guanidinium thiocyanate-phenol-chloroform extraction
TL;DR: A new method of total RNA isolation by a single extraction with an acid guanidinium thiocyanate-phenol-chloroform mixture is described, providing a pure preparation of undegraded RNA in high yield and can be completed within 4 h.
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Wall stress and patterns of hypertrophy in the human left ventricle.
TL;DR: The hypothesis that hypertrophy develops to normalize systolic but not diastolic wall stress is suggested, and it is proposed that increased syStolic tension development by myocardial fibers results in fiber thickening just sufficient to return the systolics stress (force per unit cross-sectional area) to normal.
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Molecular characterization of angiotensin II--induced hypertrophy of cardiac myocytes and hyperplasia of cardiac fibroblasts. Critical role of the AT1 receptor subtype.
Junichi Sadoshima,Seigo Izumo +1 more
TL;DR: The phenotypic changes of cardiac cells in response to Ang II in vitro closely mimic those of growth factor response in vitro and of load-induced hypertrophy in vivo, and all biological effects of Ang II examined here are mediated primarily by the AT1 receptors.
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Protooncogene induction and reprogramming of cardiac gene expression produced by pressure overload
TL;DR: Results suggest that induction of cellular protooncogenes and heat shock (stress) protein genes is an early response to pressure overload, whereas reinduction of the genes normally expressed only in perinatal life, such as fetal isoforms of contractile proteins and atrial natriuretic factor, is a later event.
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Molecular characterization of the stretch-induced adaptation of cultured cardiac cells. An in vitro model of load-induced cardiac hypertrophy.
TL;DR: The results demonstrate that the phenotype of stretched cardiocytes in this in vitro model closely mimics that of hemodynamic load-induced hypertrophy in vivo, and seems to be a suitable system with which to dissect the molecular mechanisms of load- inducedhypertrophy of cardiac muscle.