Why the study?
Advanced myocardial fibrosis in radiation-induced heart disease can cause heart failure, but its pathogenesis remains vague, with an unclarified role for DNA methylation.
This preclinical study identifies specific DNA methylation and gene expression changes in radiation-induced heart fibrosis, providing potential new therapeutic targets.
Should not change RIHD care after thoracic RT; leaves open whether promoter methylation drives or can treat late fibrosis.
Radiation-induced heart disease (RIHD) is a serious side effect of radiotherapy for thoracic tumors. Advanced myocardial fibrosis in the late phase of RIHD can lead to myocardial remodeling, heart function impairing and heart failure, resulting in serious clinical consequences, and its pathogenesis remains vague. DNA methylation is one of the important epigenetic mechanisms which often occurs in response to environmental stimuli and is crucial in regulating gene expression. We hypothesized DNA methylation may contribute to pathogenesis in radiation-induced heart fibrosis (RIHF) and altered DNA methylation patterns probably influenced the genes expression in RIHF. In present study, we found genome-wide differences in DNA methylation status and RNA expression were demonstrated and we screened out 44 genes whose altered expression maybe were regulated by CpG island methylation within the gene promoter in RIHF of Sprague-Dawley rat by employing gene expression arrays and human CpG island microarrays. Gene expression and CpG island methylation levels of several candidate genes were further validated. Our investigation provided a new dimension to reveal the specific mechanisms of RIHF and explore the potential therapeutic targets for it.
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Yao et al. (2022) studied this question.
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