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Journal ArticleDOI

Cardiac Hypertrophy: The Good, the Bad, and the Ugly

TLDR
Recent insights into hypertrophic signaling are summarized, several novel antihypertrophic strategies are considered and modulation of myocardial growth without adversely affecting contractile function is increasingly recognized as a potentially auspicious approach in the prevention and treatment of heart failure.
Abstract
Cardiac hypertrophy is the heart's response to a variety of extrinsic and intrinsic stimuli that impose increased biomechanical stress. While hypertrophy can eventually normalize wall tension, it is associated with an unfavorable outcome and threatens affected patients with sudden death or progression to overt heart failure. Accumulating evidence from studies in human patients and animal models suggests that in most instances hypertrophy is not a compensatory response to the change in mechanical load, but rather is a maladaptive process. Accordingly, modulation of myocardial growth without adversely affecting contractile function is increasingly recognized as a potentially auspicious approach in the prevention and treatment of heart failure. In this review, we summarize recent insights into hypertrophic signaling and consider several novel antihypertrophic strategies.

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Citations
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Journal ArticleDOI

A signature pattern of stress-responsive microRNAs that can evoke cardiac hypertrophy and heart failure

TL;DR: Findings reveal an important role for specific miRNAs in the control of hypertrophic growth and chamber remodeling of the heart in response to pathological signaling and point to mi RNAs as potential therapeutic targets in heart disease.
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Mammalian G proteins and their cell type specific functions

TL;DR: In this review, some of the functions of heterotrimeric G proteins in defined cells and tissues are described.
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Disruption of coordinated cardiac hypertrophy and angiogenesis contributes to the transition to heart failure

TL;DR: Both heart size and cardiac function areAngiogenesis dependent, and disruption of coordinated tissue growth and angiogenesis in the heart contributes to the progression from adaptive cardiac hypertrophy to heart failure.
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Chronic inhibition of cyclic GMP phosphodiesterase 5A prevents and reverses cardiac hypertrophy

TL;DR: It is shown that blocking the intrinsic catabolism of cGMP with an oral phosphodiesterase-5A (PDE5A) inhibitor (sildenafil) suppresses chamber and myocyte hypertrophy, and improves in vivo heart function in mice exposed to chronic pressure overload induced by transverse aortic constriction.
References
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Effects of an angiotensin-converting -enzyme inhibitor, ramipril, on cardiovascular events in high-risk patients

TL;DR: Ramipril significantly reduces the rates of death, myocardial infarction, and stroke in a broad range of high-risk patients who are not known to have a low ejection fraction or heart failure.
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Rho GTPases and the Actin Cytoskeleton

TL;DR: Members of the Rho family of small guanosine triphosphatases have emerged as key regulators of the actin cytoskeleton, and through their interaction with multiple target proteins, they ensure coordinated control of other cellular activities such as gene transcription and adhesion.
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The phosphoinositide 3-kinase pathway.

TL;DR: The PI3K pathway is implicated in human diseases including diabetes and cancer, and understanding the intricacies of this pathway may provide new avenues for therapuetic intervention.
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Prognostic Implications of Echocardiographically Determined Left Ventricular Mass in the Framingham Heart Study

TL;DR: The estimation of left ventricular mass by echocardiography offers prognostic information beyond that provided by the evaluation of traditional cardiovascular risk factors, and it is concluded that an increase in left Ventricular mass predicts a higher incidence of clinical events, including death, attributable to cardiovascular disease.
Journal ArticleDOI

Effect of metoprolol CR/XL in chronic heart failure: Metoprolol CR/XL Randomised Intervention Trial in Congestive Heart Failure (MERIT-HF)

Åke Hjalmarson, +350 more
- 12 Jun 1999 - 
TL;DR: Metoprolol controlled release/extended release (CR/XL) once daily in addition to standard therapy improved survival and the drug was well tolerated.
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