Key result
Epigenetic modifications drive cardiac fibrosis by regulating fibroblast activation and extracellular matrix deposition.
Why the study?
A comprehensive understanding of the mechanisms governing epigenetic regulation and cell crosstalk in cardiac fibrosis is critical for developing effective therapeutic strategies.
This review highlights the critical role of epigenetic regulation in cardiac fibroblasts and suggests that targeting these mechanisms could offer novel therapeutic strategies for cardiac fibrosis.
Targeting epigenetic pathways in fibroblasts remains investigational for cardiac fibrosis; leaves open clinical translation from mechanistic data.
Epigenetic mechanisms and cell crosstalk have been shown to play important roles in the initiation and progression of cardiac fibrosis. This review article aims to provide a thorough overview of the epigenetic mechanisms involved in fibroblast regulation. During fibrosis, fibroblast epigenetic regulation encompasses a multitude of mechanisms, including DNA methylation, histone acetylation and methylation, and chromatin remodeling. These mechanisms regulate the phenotype of fibroblasts and the extracellular matrix composition by modulating gene expression, thereby orchestrating the progression of cardiac fibrosis. Moreover, cardiac fibrosis disrupts normal cardiac function by imposing myocardial mechanical stress and compromising cardiac electrical conduction. This review article also delves into the intricate crosstalk between cardiomyocytes and non-cardiomyocytes in the heart. A comprehensive understanding of the mechanisms governing epigenetic regulation and cell crosstalk in cardiac fibrosis is critical for the development of effective therapeutic strategies. Further research is warranted to unravel the precise molecular mechanisms underpinning these processes and to identify potential therapeutic targets.
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Chu et al. (2023) conducted a review in Cardiac fibrosis. Epigenetic regulation was evaluated. Epigenetic mechanisms, including DNA methylation, histone modifications, and chromatin remodeling, regulate fibroblast activation and extracellular matrix deposition in the progression of cardiac fibrosis.