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Remodeling of the heart in hypertrophy in animal models with myosin essential light chain mutations

Overview of attention for article published in Frontiers in Physiology, September 2014
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Title
Remodeling of the heart in hypertrophy in animal models with myosin essential light chain mutations
Published in
Frontiers in Physiology, September 2014
DOI 10.3389/fphys.2014.00353
Pubmed ID
Authors

Katarzyna Kazmierczak, Chen-Ching Yuan, Jingsheng Liang, Wenrui Huang, Ana I. Rojas, Danuta Szczesna-Cordary

Abstract

Cardiac hypertrophy represents one of the most important cardiovascular problems yet the mechanisms responsible for hypertrophic remodeling of the heart are poorly understood. In this report we aimed to explore the molecular pathways leading to two different phenotypes of cardiac hypertrophy in transgenic mice carrying mutations in the human ventricular myosin essential light chain (ELC). Mutation-induced alterations in the heart structure and function were studied in two transgenic (Tg) mouse models carrying the A57G (alanine to glycine) substitution or lacking the N-terminal 43 amino acid residues (Δ43) from the ELC sequence. The first model represents an HCM disease as the A57G mutation was shown to cause malignant HCM outcomes in humans. The second mouse model is lacking the region of the ELC that was shown to be important for a direct interaction between the ELC and actin during muscle contraction. Our earlier studies demonstrated that >7 month old Tg-Δ43 mice developed substantial cardiac hypertrophy with no signs of histopathology or fibrosis. Tg mice did not show abnormal cardiac function compared to Tg-WT expressing the full length human ventricular ELC. Previously reported pathological morphology in Tg-A57G mice included extensive disorganization of myocytes and interstitial fibrosis with no abnormal increase in heart mass observed in >6 month-old animals. In this report we show that strenuous exercise can trigger hypertrophy and pathologic cardiac remodeling in Tg-A57G mice as early as 3 months of age. In contrast, no exercise-induced changes were noted for Tg-Δ43 hearts and the mice maintained a non-pathological cardiac phenotype. Based on our results, we suggest that exercise-elicited heart remodeling in Tg-A57G mice follows the pathological pathway leading to HCM, while it induces no abnormal response in Tg-Δ43 mice.

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Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 18 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Spain 1 6%
Unknown 17 94%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 3 17%
Researcher 3 17%
Student > Bachelor 2 11%
Student > Master 2 11%
Professor 1 6%
Other 3 17%
Unknown 4 22%
Readers by discipline Count As %
Biochemistry, Genetics and Molecular Biology 5 28%
Medicine and Dentistry 4 22%
Agricultural and Biological Sciences 1 6%
Chemistry 1 6%
Engineering 1 6%
Other 0 0%
Unknown 6 33%
Attention Score in Context

Attention Score in Context

This research output has an Altmetric Attention Score of 1. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 22 September 2014.
All research outputs
#20,237,640
of 22,764,165 outputs
Outputs from Frontiers in Physiology
#9,331
of 13,560 outputs
Outputs of similar age
#210,091
of 251,438 outputs
Outputs of similar age from Frontiers in Physiology
#82
of 127 outputs
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So far Altmetric has tracked 13,560 research outputs from this source. They typically receive more attention than average, with a mean Attention Score of 7.5. This one is in the 1st percentile – i.e., 1% of its peers scored the same or lower than it.
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