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Open AccessJournal ArticleDOI

The Right Ventricle Under Pressure: Cellular and Molecular Mechanisms of Right-Heart Failure in Pulmonary Hypertension

TLDR
This overview identifies the gaps in the understanding of RV failure and attempts to fill them, when possible, and aims to encourage the pulmonary hypertension research community to direct some of their attention to the RV, in parallel to their focus on the pulmonary vasculature.
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This article is published in Chest.The article was published on 2009-03-01 and is currently open access. It has received 627 citations till now. The article focuses on the topics: Pressure overload & Afterload.

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Citations
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Journal ArticleDOI

Mechanisms of disease: pulmonary arterial hypertension

TL;DR: Perturbations of a number of molecular mechanisms have been described, including pathways involving growth factors, cytokines, metabolic signaling, elastases, and proteases, that may underlie the pathogenesis of the disease.
Journal ArticleDOI

Chronic Pulmonary Artery Pressure Elevation Is Insufficient to Explain Right Heart Failure

TL;DR: In this article, a mechanical animal model of chronic progressive pulmonary arterial pressure overload (pulmonary artery banding, not associated with structural alterations of the lung circulation) was compared with an established model of angioproliferative pulmonary hypertension associated with fatal RV failure.
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The monocrotaline model of pulmonary hypertension in perspective

TL;DR: Although the monocrotaline rat model of PAH has contributed to a better understanding of vascular remodeling in pulmonary hypertension, the validity of this model as a preclinically relevant model of severe plexogenic PAH is questioned.
Journal ArticleDOI

Anatomy, Function, and Dysfunction of the Right Ventricle: JACC State-of-the-Art Review

TL;DR: Current knowledge of the right ventricle (RV) anatomic, structural, metabolic,functional, functional, and hemodynamic characteristics in both health and disease is summarized.
References
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Journal ArticleDOI

The effect of spironolactone on morbidity and mortality in patients with severe heart failure. Randomized Aldactone Evaluation Study Investigators.

TL;DR: Blockade of aldosterone receptors by spironolactone, in addition to standard therapy, substantially reduces the risk of both morbidity and death among patients with severe heart failure.
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Bone marrow cells regenerate infarcted myocardium

TL;DR: It is indicated that locally delivered bone marrow cells can generate de novo myocardium, ameliorating the outcome of coronary artery disease.
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Adult Cardiac Stem Cells Are Multipotent and Support Myocardial Regeneration

TL;DR: The existence of Lin(-) c-kit(POS) cells with the properties of cardiac stem cells, which are self-renewing, clonogenic, and multipotent, giving rise to myocytes, smooth muscle, and endothelial cells are reported.
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