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Transforming growth factor-β-mediated CD44/STAT3 signaling contributes to the development of atrial fibrosis and fibrillation

Overview of attention for article published in Basic Research in Cardiology, September 2017
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  • Above-average Attention Score compared to outputs of the same age (62nd percentile)
  • Average Attention Score compared to outputs of the same age and source

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5 X users
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1 Facebook page

Citations

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30 Mendeley
Title
Transforming growth factor-β-mediated CD44/STAT3 signaling contributes to the development of atrial fibrosis and fibrillation
Published in
Basic Research in Cardiology, September 2017
DOI 10.1007/s00395-017-0647-9
Pubmed ID
Authors

Shang-Hung Chang, Yung-Hsin Yeh, Jia-Lin Lee, Yu-Juei Hsu, Chi-Tai Kuo, Wei-Jan Chen

Abstract

Atrial fibrillation (AF) is associated with atrial fibrosis. Inhibition of atrial fibrosis might be a plausible approach for AF prevention and therapy. This study is designed to evaluate the potential role of CD44, a membrane receptor known to regulate fibrosis, and its related signaling in the pathogenesis of atrial fibrosis and AF. Treatment of cultured rat atrial fibroblasts with transforming growth factor-β (TGF-β, a key mediator of atrial fibrosis) led to a higher expression of hyaluronan (HA), CD44, STAT3, and collagen (a principal marker of fibrosis) than that of ventricular fibroblasts. In vivo, TGF-β transgenic mice and AF patients exhibited a greater expression of HA, CD44, STAT3, and collagen in their atria than wild-type mice and sinus rhythm subjects, respectively. Treating TGF-β transgenic mice with an anti-CD44 blocking antibody resulted in a lower expression of STAT3 and collagen in their atria than those with control IgG antibody. Programmed stimulation triggered less AF episodes in TGF-β transgenic mice treated with anti-CD44 blocking antibody than in those with control IgG. Blocking CD44 signaling with anti-CD44 antibody and mutated CD44 plasmids attenuated TGF-β-induced STAT3 activation and collagen expression in cultured atrial fibroblasts. Deletion and mutational analysis of the collagen promoter along with chromatin immunoprecipitation demonstrated that STAT3 served as a vital transcription factor in collagen expression. TGF-β-mediated HA/CD44/STAT3 pathway plays a crucial role in the development of atrial fibrosis and AF. Blocking CD44-dependent signaling may be a feasible way for AF management.

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X Demographics

The data shown below were collected from the profiles of 5 X users who shared this research output. Click here to find out more about how the information was compiled.
Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 30 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 30 100%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 5 17%
Student > Master 4 13%
Other 3 10%
Student > Bachelor 3 10%
Professor > Associate Professor 2 7%
Other 2 7%
Unknown 11 37%
Readers by discipline Count As %
Medicine and Dentistry 5 17%
Biochemistry, Genetics and Molecular Biology 2 7%
Immunology and Microbiology 2 7%
Neuroscience 2 7%
Computer Science 1 3%
Other 5 17%
Unknown 13 43%
Attention Score in Context

Attention Score in Context

This research output has an Altmetric Attention Score of 4. 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 12 September 2017.
All research outputs
#7,438,886
of 23,001,641 outputs
Outputs from Basic Research in Cardiology
#177
of 651 outputs
Outputs of similar age
#118,212
of 315,686 outputs
Outputs of similar age from Basic Research in Cardiology
#4
of 8 outputs
Altmetric has tracked 23,001,641 research outputs across all sources so far. This one has received more attention than most of these and is in the 67th percentile.
So far Altmetric has tracked 651 research outputs from this source. They receive a mean Attention Score of 5.0. This one has gotten more attention than average, scoring higher than 72% of its peers.
Older research outputs will score higher simply because they've had more time to accumulate mentions. To account for age we can compare this Altmetric Attention Score to the 315,686 tracked outputs that were published within six weeks on either side of this one in any source. This one has gotten more attention than average, scoring higher than 62% of its contemporaries.
We're also able to compare this research output to 8 others from the same source and published within six weeks on either side of this one. This one has scored higher than 4 of them.