Key result
Targeting epigenetic modifications offers reversible strategies to attenuate cardiac fibroblast activation and myocardial fibrosis.
Why the study?
Emerging evidence highlights the significant involvement of epigenetic regulation in cardiac fibroblast activation, cardiac fibrosis, and myocardial dysfunction.
This narrative review synthesizes the molecular mechanisms by which DNA methylation, histone modifications, and non-coding RNAs regulate cardiac fibroblast activation, highlighting the therapeutic potential of epigenetic drugs to reverse myocardial fibrosis.
Epigenetic drugs for fibrosis should not yet change practice; leaves open prospective trials to test reversibility.
Myocardial fibroblasts play a crucial role in heart structure and function. In recent years, significant progress has been made in understanding the epigenetic regulation of myocardial fibroblasts, which is essential for cardiac development, homeostasis, and disease progression. In healthy hearts, cardiac fibroblasts (CFs) play a crucial role in synthesizing the extracellular matrix (ECM) when in a dormant state. However, under pathological and environmental stress, CFs transform into activated fibroblasts known as myofibroblasts. These myofibroblasts produce an excess of ECM, which promotes cardiac fibrosis. Although multiple molecular mechanisms are associated with CF activation and myocardial dysfunction, emerging evidence highlights the significant involvement of epigenetic regulation in this process. Epigenetics refers to the heritable changes in gene expression that occur without altering the DNA sequence. These mechanisms have emerged as key regulators of myocardial fibroblast function. This review focuses on recent advancements in the understanding of the role of epigenetic regulation and emphasizes the impact of epigenetic modifications on CF activation. Furthermore, we present perspectives and prospects for future research on epigenetic modifications and their implications for myocardial fibroblasts.
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Komal et al. (2024) conducted a review in Myocardial fibrosis and cardiovascular diseases. Epigenetic regulation and epigenetic drugs (e.g., DNMT inhibitors, HDAC inhibitors, HMT inhibitors, non-coding RNA-targeted therapies) was evaluated on Cardiac fibroblast activation and myocardial fibrosis progression. Epigenetic modifications, including DNA methylation, histone modifications, and non-coding RNAs, critically regulate cardiac fibroblast activation and offer reversible targets for myocardial fibrosis.
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