Literature DB >> 12555129

Concentric versus eccentric remodeling.

Blase A Carabello1.   

Abstract

Cardiac hypertrophy has long been recognized as one of the heart's mechanisms for compensating a pressure or volume overload. This compensation has often been viewed as a feedback loop in which the concentric hypertrophy, which develops in pressure overload, normalizes wall stress while the eccentric hypertrophy, which develops in volume overload, allows for an increase in total stroke volume to compensate that which is lost from regulation. While the concentric hypertrophy of pressure overload often is compensatory, many examples are noted where either too little hypertrophy occurs to normalize stress or in other cases, in which hypertrophy exceeds the amount needed for normalization. These observations invoke nonmechanical mechanisms which modulate the degree to which the mechanical signal of pressure overload is translated into an increase in myocardial mass. Hypertrophy develops when the rate of myocardial protein synthesis exceeds that of protein degradation. It now appears that in pressure overload this imbalance is created as synthesis rate increases while in volume overload hypertrophy appears to accrue because degradation rate decreases.

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Mesh:

Year:  2002        PMID: 12555129     DOI: 10.1054/jcaf.2002.129250

Source DB:  PubMed          Journal:  J Card Fail        ISSN: 1071-9164            Impact factor:   5.712


  26 in total

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Review 2.  Cardiac remodeling and subcellular defects in heart failure due to myocardial infarction and aging.

Authors:  Naranjan S Dhalla; Shashanka Rangi; Andrea P Babick; Shelley Zieroth; Vijayan Elimban
Journal:  Heart Fail Rev       Date:  2012-09       Impact factor: 4.214

3.  Suppression of class I and II histone deacetylases blunts pressure-overload cardiac hypertrophy.

Authors:  Yongli Kong; Paul Tannous; Guangrong Lu; Kambeez Berenji; Beverly A Rothermel; Eric N Olson; Joseph A Hill
Journal:  Circulation       Date:  2006-05-30       Impact factor: 29.690

4.  Cardiac copper deficiency activates a systemic signaling mechanism that communicates with the copper acquisition and storage organs.

Authors:  Byung-Eun Kim; Michelle L Turski; Yasuhiro Nose; Michelle Casad; Howard A Rockman; Dennis J Thiele
Journal:  Cell Metab       Date:  2010-05-05       Impact factor: 27.287

5.  Long-term effects of epoprostenol on the pulmonary vasculature in idiopathic pulmonary arterial hypertension.

Authors:  Stuart Rich; Jennifer Pogoriler; Aliya N Husain; Peter T Toth; Mardi Gomberg-Maitland; Stephen L Archer
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Review 6.  Endocrine and other physiologic modulators of perinatal cardiomyocyte endowment.

Authors:  S S Jonker; S Louey
Journal:  J Endocrinol       Date:  2015-10-02       Impact factor: 4.286

7.  In vivo measurements of the contributions of protein synthesis and protein degradation in regulating cardiac pressure overload hypertrophy in the mouse.

Authors:  Paul J McDermott; Catalin F Baicu; Shaun R Wahl; An O Van Laer; Michael R Zile
Journal:  Mol Cell Biochem       Date:  2012-05-19       Impact factor: 3.396

8.  Systemic arterial hypertension but not IGF-I treatment stimulates cardiomyocyte enlargement in neonatal lambs.

Authors:  Adrienne N Wilburn; George D Giraud; Samantha Louey; Terry Morgan; Nainesh Gandhi; Sonnet S Jonker
Journal:  Am J Physiol Regul Integr Comp Physiol       Date:  2018-09-12       Impact factor: 3.619

9.  Right ventricular remodeling in response to volume overload in fetal sheep.

Authors:  Tara Karamlou; George D Giraud; Donogh McKeogh; Sonnet S Jonker; Irving Shen; Ross M Ungerleider; Kent L Thornburg
Journal:  Am J Physiol Heart Circ Physiol       Date:  2019-02-01       Impact factor: 4.733

10.  Cardiac and renal function are progressively impaired with aging in Zucker diabetic fatty type II diabetic rats.

Authors:  John Baynes; David B Murray
Journal:  Oxid Med Cell Longev       Date:  2009 Nov-Dec       Impact factor: 6.543

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