Autocrine release of angiotensin II mediates stretch-induced hypertrophy of cardiac myocytes in vitro
TLDR
Using an in vitro model of load (stretch)-induced cardiac hypertrophy, it is demonstrated that mechanical stretch causes release of angiotensin II (Ang II) from cardiac myocytes and that Ang II acts as an initial mediator of the stretch-induced hypertrophic response.About:
This article is published in Cell.The article was published on 1993-12-03 and is currently open access. It has received 1354 citations till now. The article focuses on the topics: Angiotensin II & Cardiac muscle.read more
Citations
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Journal ArticleDOI
A Calcineurin-Dependent Transcriptional Pathway for Cardiac Hypertrophy
Jeffery D. Molkentin,Jeffery D. Molkentin,Jianrong Lu,Christopher L. Antos,Bruce E. Markham,James A. Richardson,Jeffrey Robbins,Stephen R. Grant,Eric N. Olson +8 more
TL;DR: It is shown that cardiac hypertrophy is induced by the calcium-dependent phosphatase calcineurin, which dephosphorylates the transcription factor NF-AT3, enabling it to translocate to the nucleus.
Journal ArticleDOI
Cardiac remodeling—concepts and clinical implications: a consensus paper from an international forum on cardiac remodeling
TL;DR: Left ventricular end-diastolic and end-systolic volume and ejection fraction data provide support for the beneficial effects of therapeutic agents such as angiotensin-converting enzyme (ACE) inhibitors and beta-adrenergic blocking agents on the remodeling process.
Journal ArticleDOI
Tensegrity: the architectural basis of cellular mechanotransduction
TL;DR: This review attempts to place the potential molecular mediators of mechanotransduction (e.g. stretch-sensitive ion channels, signaling molecules, cytoskeleton, integrins) within the context of the structural complexity of living cells.
Journal ArticleDOI
Physiology of local renin-angiotensin systems.
TL;DR: A large body of data is now available to support the existence of numerous organ-based RAS exerting diverse physiological effects, and universal paracrine and autocrine actions may be important in many organ systems and can mediate important physiological stimuli.
Journal ArticleDOI
Cellular mechanotransduction: putting all the pieces together again.
TL;DR: Future research in this area will require analysis, understanding, and modeling of tensionally integrated systems of mechanochemical control, and the presence of isometric tension at all levels of these multiscale networks ensures that various molecular scale mechanochemical transduction mechanisms proceed simultaneously and produce a concerted response.
References
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Journal ArticleDOI
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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Effect of captopril on progressive ventricular dilatation after anterior myocardial infarction.
TL;DR: It is indicated that after anterior myocardial infarction, ventricular enlargement is progressive and that captopril may attenuate this process, reduce filling pressures, and improve exercise tolerance.
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Constitutive and Regulated Secretion of Proteins
TL;DR: SORTing 257 CYTOSKELETON INVOLVEMENT with PROTEIN SECRETION 266SECRETION in EPITHELIAL CELLS 277 RECYCLING of the SECRETORY VESICLE MEMBRANE 281
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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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Regulation of cardiac gene expression during myocardial growth and hypertrophy: molecular studies of an adaptive physiologic response.
TL;DR: The development of a bona fide in vivo pressure overload model of hypertrophy in a small animal model that can be genetically manipulated should allow a rigorous analysis of the role of specific signaling mechanisms in the activation of the responses of cardiac genes during the hypertrophic process in vivo.
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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.
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