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miR‐130 aggravates acute myocardial infarction‐induced myocardial injury by targeting PPAR‐γ

Overview of attention for article published in Journal of Cellular Biochemistry, May 2018
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Title
miR‐130 aggravates acute myocardial infarction‐induced myocardial injury by targeting PPAR‐γ
Published in
Journal of Cellular Biochemistry, May 2018
DOI 10.1002/jcb.26903
Pubmed ID
Authors

Xianglin Chu, Yiqing Wang, Liewen Pang, Jiechun Huang, Xiaotian Sun, Xiaofeng Chen

Abstract

Cardiac remodeling is a common pathophysiological change associated with acute myocardial infarction (AMI). Recent evidence indicates that microRNAs are strong posttranscriptional regulators which play an important role in regulating the microenvironment of myocardial tissue after AMI. In this study, we sought to explore the potential role and underlying mechanism of miR-130 in AMI. H9c2 cells were cultured under hypoxic conditions to simulate myocardial infarction. The influence of aberrantly expressed miR-130 on H9c2 cells under hypoxia was also estimated with RT-PCR, western blot and enzyme-linked immunosorbent assay. Using bioinformatics methods, of miR-130 target genes were verified with luciferase reporter assay. Then, the effects of miR-130 on AMI were identified in an induced myocardial injury model in rats. The results show that miR-130 downregulation remarkably decreased hypoxia-induced inflammation and fibrosis related protein expression in H9c2 cells and reversed hypoxia-induced peroxisome proliferator-activated receptor γ (PPAR-γ) inhibition. A bifluorescein reporter assay further confirmed that PPAR-γ was a target gene of miR-130. This study verified that PPAR-γ has a cardioprotective effect by inhibiting NFκB-mediated inflammation and TGF-β1-mediated fibrosis. In vivo experiments confirmed that downregulation of miR-130 expression promotes PPAR-γ-mediated cardioprotective effects by suppressing inflammation and myocardial fibrosis. Taken together, these findings suggest that miR-130 knockdown alleviates infarction-induced myocardial injury by promoting PPAR-γ expression.

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Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 27 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 27 100%

Demographic breakdown

Readers by professional status Count As %
Student > Bachelor 3 11%
Researcher 3 11%
Student > Ph. D. Student 3 11%
Lecturer > Senior Lecturer 2 7%
Other 1 4%
Other 5 19%
Unknown 10 37%
Readers by discipline Count As %
Biochemistry, Genetics and Molecular Biology 3 11%
Medicine and Dentistry 2 7%
Psychology 2 7%
Pharmacology, Toxicology and Pharmaceutical Science 1 4%
Nursing and Health Professions 1 4%
Other 5 19%
Unknown 13 48%
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 16 May 2018.
All research outputs
#20,492,220
of 23,055,429 outputs
Outputs from Journal of Cellular Biochemistry
#3,810
of 4,734 outputs
Outputs of similar age
#287,327
of 326,939 outputs
Outputs of similar age from Journal of Cellular Biochemistry
#65
of 112 outputs
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We're also able to compare this research output to 112 others from the same source and published within six weeks on either side of this one. This one is in the 1st percentile – i.e., 1% of its contemporaries scored the same or lower than it.