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Aldehyde dehydrogenase-2 protects against myocardial infarction-related cardiac fibrosis through modulation of the Wnt/β-catenin signaling pathway

Overview of attention for article published in Therapeutics and Clinical Risk Management, September 2015
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About this Attention Score

  • Good Attention Score compared to outputs of the same age (70th percentile)
  • Good Attention Score compared to outputs of the same age and source (72nd percentile)

Mentioned by

twitter
2 tweeters
wikipedia
2 Wikipedia pages

Citations

dimensions_citation
34 Dimensions

Readers on

mendeley
26 Mendeley
Title
Aldehyde dehydrogenase-2 protects against myocardial infarction-related cardiac fibrosis through modulation of the Wnt/β-catenin signaling pathway
Published in
Therapeutics and Clinical Risk Management, September 2015
DOI 10.2147/tcrm.s88297
Pubmed ID
Authors

Yingchun Zhou, Xinjun Zhao, Yue Hua, Hongmei Chen, Haiyu Yang, Tao Zhang, Guiqiong Huang, Huijie Fan, Zhangbin Tan, Xiaofang Huang, Bin Liu

Abstract

Aldehyde dehydrogenase-2 (ALDH2) has a protective effect on ischemic heart disease. Here, we examined the protective effects of ALDH2 on cardiac fibrosis through modulation of the Wnt/β-catenin signaling pathway in a rat model of myocardial infarction (MI). Wistar rats were divided into the sham (control), MI (model), and ALDH2 activator (Alda-1) groups. After 10 days of treatment, the left ventricular (LV) remodeling parameters of each animal were evaluated by echocardiography. Myocardial fibrosis was evaluated by Masson's trichrome staining and Sirius Red staining. Expression levels of collagen types I and III and α-smooth muscle actin (α-SMA) were examined. Finally, the expression and activity of ALDH2 and the levels of several Wnt-related proteins and genes, such as phosphoglycogen synthase kinase (GSK)-3β, GSK-3β, β-catenin, Wnt-1, WNT1-inducible signaling-pathway protein 1, and tumor necrosis factor (TNF)-α, were also analyzed. After MI, the heart weight/body weight ratio, LV dimension at end diastole, and LV dimension at end systole were decreased, while the LV ejection fraction and LV fractional shortening were increased in the Alda-1 group. Myocardial fibrosis was also reduced in the Alda-1 group, accompanied by decreased expression collagen types I and III and α-SMA. β-Catenin, phosphorylated GSK-3β, and Wnt-1 levels were significantly increased in the model group. Interestingly, this alteration was partly reversed by Alda-1 treatment. Immunohistochemical staining showed that numerous WNT1-inducible signaling-pathway protein 1 (WISP-1)- and TNF-α-positive cells were found in the model group. However, few WISP-1- and TNF-α-positive cells were detected in the Alda-1 group. The reduction of cardiac fibrosis and the down-regulation of β-catenin, phosphorylated GSK-3β, Wnt-1, and WISP-1 may be mediated by increased ALDH2 activity, leading to reduction of MI-related cardiac fibrosis.

Twitter Demographics

The data shown below were collected from the profiles of 2 tweeters who shared this research output. Click here to find out more about how the information was compiled.

Mendeley readers

The data shown below were compiled from readership statistics for 26 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
United Kingdom 1 4%
Unknown 25 96%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 6 23%
Student > Bachelor 4 15%
Researcher 3 12%
Student > Postgraduate 2 8%
Student > Master 2 8%
Other 3 12%
Unknown 6 23%
Readers by discipline Count As %
Medicine and Dentistry 6 23%
Agricultural and Biological Sciences 4 15%
Biochemistry, Genetics and Molecular Biology 3 12%
Pharmacology, Toxicology and Pharmaceutical Science 2 8%
Social Sciences 2 8%
Other 2 8%
Unknown 7 27%

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 20 September 2017.
All research outputs
#6,425,431
of 22,828,180 outputs
Outputs from Therapeutics and Clinical Risk Management
#336
of 1,264 outputs
Outputs of similar age
#75,940
of 266,861 outputs
Outputs of similar age from Therapeutics and Clinical Risk Management
#17
of 62 outputs
Altmetric has tracked 22,828,180 research outputs across all sources so far. This one has received more attention than most of these and is in the 70th percentile.
So far Altmetric has tracked 1,264 research outputs from this source. They typically receive more attention than average, with a mean Attention Score of 8.5. 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 266,861 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 70% of its contemporaries.
We're also able to compare this research output to 62 others from the same source and published within six weeks on either side of this one. This one has gotten more attention than average, scoring higher than 72% of its contemporaries.