ArticleBMC cardiovascular disorders2019
The expression profile analysis of atrial mRNA in rats with atrial fibrillation: the role of IGF1 in atrial fibrosis.
Article in BMC cardiovascular disorders, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed, 13 citations in OpenAlex.
- Atrial fibrillation: the role of hypoxia-inducible factor-1-regulated cytokines.Molecular and cellular biochemistry · 2021Review
- Cardiac Pressure Overload Decreases ETV1 Expression in the Left Atrium, Contributing to Atrial Electrical and Structural Remodeling.Circulation · 2021Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundStructural remodeling is critical to the initiation and maintenance of atrial fibrillation (AF). IGF1, insulin like growth factor 1, has been recognized as contributor to fibrosis. However, the roles and mechanisms of IGF1 in structural remodeling during AF is still unclear.
methodsWe investigated the transcriptional expression profiles of left atria in AF and non-AF rat models by using microarray analysis. And quantitative real-time polymerase chain reaction (qRT-PCR) was performed to validate the accuracy. After bioinformatics analysis, IGF1 was selected to explore its effects and mechanisms on atrial fibrosis. The fibroblasts were extracted from atria of rats, and randomly divided into negative control group, mIGF1 overexpression group and mIGF1 silencing group. Then 30 healthy male Wistar rats were randomly divided into negative control group (n = 10), pacing group (n = 10), pacing + mIGF1 silencing viruses group (n = 10). Then the intracardiac electrophysiological examination, qRT-PCR, Western Blotting, masson staining were conducted after IGF1 interfering experiments.
resultsA total of 956 differentially expressed transcripts were identified, in which 395 transcripts were down-regulated and 561 transcripts were up-regulated. Bioinformatics analysis was conducted to predict the functions and interactions of the aberrantly expressed genes. The inhibition of IGF1 function in AF model could ameliorate the inducibility of AF. The IGF1 plays a fibrotic role by activating the PI3K-Akt pathway to increase the expression of CTGF and AT1R.
conclusionsIGF1 develops vital function in regulating structural remodeling during AF, which could illustrate the mechanism of AF pathogenesis and supply potential targets for its precise treatment.
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