AI Article Synopsis
- N6-adenosine methylation (m6A) is identified as a significant RNA modification linked to heart failure, with specific miRNAs potentially influencing this process.
- Analysis of transcriptome and methylation data in mice led to the identification of key m6A enzymes involved in heart failure, highlighting their connection with differentially expressed miRNAs.
- The study concludes that miR-23b-3p and let-7b-5p could regulate RNA methylation through these enzymes, offering insights for potential therapeutic approaches for heart failure.
Article Abstract
Background: N6-adenosine methylation (m6A) is a prevalent RNA modification associated with heart failure, alongside aberrant miRNA expression. Despite indications of miRNAs regulating m6A modification, their specific influence on m6A in heart failure remains unclear.
Methods: The initial analysis utilized transcriptome and methylation sequencing data from GSE131296 in mice to identify key m6A methylation enzymes in heart failure and construct an associated network. Integration of miRNA sequencing data from GSE231700 revealed miRNAs influencing m6A methylation enzymes, contributing to the formation of a comprehensive network. Furthermore, differential miRNA levels in human serum were assessed via qPCR, and the expression of m6A methyltransferases in the heart was confirmed using proteomic databases.
Results: In pressure overload-induced heart failure mice, 217 mRNAs showed differential expression, with FTO and IGF2BP2 identified as m6A methylation enzymes. Subsequent methylation sequencing revealed 884 highly-methylated and 178 lowly-methylated peaks, establishing a network linking Fto and Igf2bp2 with these peaks. Additionally, miRNA sequencing identified 156 differentially expressed miRNAs, including let-7b-5p and miR-23b-3p, predicted as m6Aregulating miRNAs, both elevated in heart failure patients.
Conclusion: miR-23b-3p and let-7b-5p are identified as potential regulators of RNA methylation in heart failure, acting via FTO and IGF2BP2, offering new insights into the role of miRNA-mediated RNA methylation and its potential therapeutic avenues for heart failure.
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| http://dx.doi.org/10.2174/0113862073316437240426071022 | DOI Listing |
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