ArticleThe American journal of pathology2010
Temporal evaluation of cardiac myocyte hypertrophy and hyperplasia in male rats secondary to chronic volume overload.
Article in The American journal of pathology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 37 citations in OpenAlex.
- Gestational exposure to micro and nanoplastics differentially impacts cardiac development and function in male and female rats throughout the lifespan.Toxicology and applied pharmacology · 2025Article
- Contributions of mechanical loading and hormonal changes to eccentric hypertrophy during volume overload: A Bayesian analysis using logic-based network models.PLoS computational biology · 2025Article
- Acute exposure to LPS induces cardiac dysfunction via the activation of the NLRP3 inflammasome.Scientific reports · 2024Article
- Impaired renal autoregulation and pressure-natriuresis: any role in the development of heart failure in normotensive and angiotensin II-dependent hypertensive rats?Hypertension research : official journal of the Japanese Society of Hypertension · 2023Article
- Automatic Quantification of Cardiomyocyte Dimensions and Connexin 43 Lateralization in Fluorescence Images.Biomolecules · 2020Article
- Formulation and Characterization of Solid Lipid Nanoparticles Loading RF22-c, a Potent and Selective 5-LO Inhibitor, in a Monocrotaline-Induced Model of Pulmonary Hypertension.Frontiers in pharmacology · 2020Article
- Article
- Can the echocardiographic LV mass equation reliably demonstrate stable LV mass following acute change in LV load?Annals of translational medicine · 2019Article
- Sex differences in volume overload in skinned fibers.BMC cardiovascular disorders · 2016Article
- Differential Effects of Prevention and Reversal Treatment with Lisinopril on Left Ventricular Remodelling in a Rat Model of Heart Failure.Heart, lung & circulation · 2015Article
- Trpm4 gene invalidation leads to cardiac hypertrophy and electrophysiological alterations.PloS one · 2014Article
- Temporal changes in integrin-mediated cardiomyocyte adhesion secondary to chronic cardiac volume overload in rats.American journal of physiology. Heart and circulatory physiology · 2014Article
- Gender differences in non-ischemic myocardial remodeling: are they due to estrogen modulation of cardiac mast cells and/or membrane type 1 matrix metalloproteinase.Pflugers Archiv : European journal of physiology · 2013Review
- Estrogenic modulation of inflammation-related genes in male rats following volume overload.Physiological genomics · 2012Article
- Cardiac proteasome activity in muscle ring finger-1 null mice at rest and following synthetic glucocorticoid treatment.American journal of physiology. Endocrinology and metabolism · 2011Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
The temporal myocardial remodeling induced by chronic ventricular volume overload in male rats was examined. Specifically, left ventricular (LV) cardiomyocyte length and width, sarcomere length, and number of nuclei were measured in male rats (n = 8 to 17) at 1, 3, 5, 7, 21, 35, and 56 days after creation of an infrarenal aortocaval fistula. In contrast to previously published reports of progressive increases in cardiomyocyte length and cross-sectional area at 5 days post-fistula and beyond in female hearts, cardiomyocyte length and width did not increase significantly in males during the first 35 days of volume overload. Furthermore, a significant decrease in cardiomyocyte length relative to age-matched controls, together with a reduced number of sarcomeres per cell, was noted in male hearts at 5 days post-fistula. There was a concurrent increase in the percentage of mononucleated cardiomyocytes from 11.6% to 18% at 5 days post-fistula. These initial differences could not be attributed to cardiomyocyte proliferation, and treatment with a microtubule stabilizing agent prevented them from occurring. The subsequent significant increase in LV weight without corresponding increases in cardiomyocyte dimensions is indicative of hyperplasia. Thus, these findings indicate hyperplasia resulting from cytokinesis of cardiomyocytes is a key mechanism, independent of hypertrophy, that contributes to the significant increase in LV mass in male hearts subjected to chronic volume overload.
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