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Citations to this article

Intermittent pressure overload triggers hypertrophy-independent cardiac dysfunction and vascular rarefaction
Cinzia Perrino, … , Oliver Smithies, Howard A. Rockman
Cinzia Perrino, … , Oliver Smithies, Howard A. Rockman
Published June 1, 2006
Citation Information: J Clin Invest. 2006;116(6):1547-1560. https://doi.org/10.1172/JCI25397.
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Research Article Cardiology Article has an altmetric score of 12

Intermittent pressure overload triggers hypertrophy-independent cardiac dysfunction and vascular rarefaction

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Abstract

For over a century, there has been intense debate as to the reason why some cardiac stresses are pathological and others are physiological. One long-standing theory is that physiological overloads such as exercise are intermittent, while pathological overloads such as hypertension are chronic. In this study, we hypothesized that the nature of the stress on the heart, rather than its duration, is the key determinant of the maladaptive phenotype. To test this, we applied intermittent pressure overload on the hearts of mice and tested the roles of duration and nature of the stress on the development of cardiac failure. Despite a mild hypertrophic response, preserved systolic function, and a favorable fetal gene expression profile, hearts exposed to intermittent pressure overload displayed pathological features. Importantly, intermittent pressure overload caused diastolic dysfunction, altered β-adrenergic receptor (βAR) function, and vascular rarefaction before the development of cardiac hypertrophy, which were largely normalized by preventing the recruitment of PI3K by βAR kinase 1 to ligand-activated receptors. Thus stress-induced activation of pathogenic signaling pathways, not the duration of stress or the hypertrophic growth per se, is the molecular trigger of cardiac dysfunction.

Authors

Cinzia Perrino, Sathyamangla V. Naga Prasad, Lan Mao, Takahisa Noma, Zhen Yan, Hyung-Suk Kim, Oliver Smithies, Howard A. Rockman

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Total citations by year

Year: 2025 2024 2023 2022 2021 2020 2019 2018 2017 2016 2015 2014 2013 2012 2011 2010 2009 2008 2007 2006 Total
Citations: 2 4 10 8 10 3 5 5 8 5 12 6 6 5 6 5 10 2 6 1 119
Citation information
This citation data is accumulated from CrossRef, which receives citation information from participating publishers, including this journal. Not all publishers participate in CrossRef, so this information is not comprehensive. Additionally, data may not reflect the most current citations to this article, and the data may differ from citation information available from other sources (for example, Google Scholar, Web of Science, and Scopus).

Citations to this article in year 2009 (10)

Title and authors Publication Year
Endogenous S-nitrosothiols protect against myocardial injury
B Lima, GK Lam, L Xie, DL Diesen, N Villamizar, J Nienaber, E Messina, D Bowles, CD Kontos, JM Hare, JS Stamler, HA Rockman
Proceedings of the National Academy of Sciences 2009
Pulmonary surfactant: an immunological perspective
ZC Chroneos, Z Sever-Chroneos, VL Shepherd
Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology 2009
 1-Adrenergic receptors stimulate cardiac contractility and CaMKII activation in vivo and enhance cardiac dysfunction following myocardial infarction
B Yoo, A Lemaire, S Mangmool, MJ Wolf, A Curcio, L Mao, HA Rockman
American journal of physiology. Heart and circulatory physiology 2009
Reduced Phosphoinositide 3-Kinase (p110α) Activation Increases the Susceptibility to Atrial Fibrillation
L Pretorius, XJ Du, EA Woodcock, H Kiriazis, RC Lin, S Marasco, RL Medcalf, Z Ming, GA Head, JW Tan, N Cemerlang, J Sadoshima, T Shioi, S Izumo, EV Lukoshkova, AM Dart, GL Jennings, JR McMullen
The American Journal of Pathology 2009
Decreased beta-adrenergic responsiveness following hypertrophy occurs only in cardiomyocytes that also re-express beta-myosin heavy chain
K Pandya, K Porter, HA Rockman, O Smithies
European Journal of Heart Failure 2009
TRPC1 channels are critical for hypertrophic signaling in the heart
M Seth, ZS Zhang, L Mao, V Graham, J Burch, J Stiber, L Tsiokas, M Winn, J Abramowitz, HA Rockman, L Birnbaumer, P Rosenberg
Circulation research 2009
Tissue doppler imaging can be useful to distinguish pathological from physiological left ventricular hypertrophy: a study in master athletes and mild hypertensive subjects
G Galanti, L Toncelli, FD Furia, L Stefani, B Cappelli, AD Luca, MC Vono
Cardiovascular ultrasound 2009
Contractility and ventricular systolic stiffening in hypertensive heart disease insights into the pathogenesis of heart failure with preserved ejection fraction
BA Borlaug, CS Lam, VL Roger, RJ Rodeheffer, MM Redfield
Journal of the American College of Cardiology 2009
Nasal vaccination with troponin reduces troponin specific T-cell responses and improves heart function in myocardial ischemia-reperfusion injury
D Frenkel, AS Pachori, L Zhang, A Dembinsky-Vaknin, D Farfara, S Petrovic-Stojkovic, VJ Dzau, HL Weiner
International Immunology 2009
 -Arrestin Mediates  1-Adrenergic Receptor-Epidermal Growth Factor Receptor Interaction and Downstream Signaling
DG Tilley, IM Kim, PA Patel, JD Violin, HA Rockman
The Journal of biological chemistry 2009

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