Epigenetic Regulatory Networks in Cardiac Fibrosis: Therapeutic Targets, Crosstalk, and Future Directions.
- 1School of Basic Medicine Sciences, Zhejiang Chinese Medical University, Hangzhou, Zhejiang, People's Republic of China.
- 2College of Chinese Medicine for Cardiovascular-Cranial Disease, Zhejiang Chinese Medical University, Hangzhou, Zhejiang, People's Republic of China.
- 3Zhejiang Key Laboratory of Chinese Medicine for Cardiovascular and Cerebrovascular Disease, Hangzhou, Zhejiang, People's Republic of China.
Abstract
Cardiac fibrosis is a central driver of pathological cardiac remodeling and a critical risk factor for the progression to heart failure. Cardiac fibrosis may induce myocardial ischemia and hypoxia, impaired cardiac function, and arrhythmias, and is thereby intimately linked to escalating cardiac mortality. Epigenetic mechanisms serve as core drivers in both the initiation and malignant evolution of cardiac fibrosis. Currently, the epigenetic regulatory network primarily covers five cutting-edge domains: (1) dynamic DNA methylation modifications, (2) the histone post-translational modifications, (3) emerging RNA epitranscriptomic modifications, (4) the non-coding RNA regulatory network, and (5) ATP-dependent chromatin remodeling. This review moves beyond conventional pathological frameworks to examine the multi-layered synergistic actions of epigenetic regulation in cardiac fibrosis. By deconstructing the specific spatiotemporal expression profiles of these dynamic modification mechanisms, we systematically evaluate their translational potential as reversible interventional targets, offering a critical synthesis of these epigenetic mechanisms and pointing to plausible research directions for overcoming fibrotic progression toward heart failure.
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BibTeX
@article{yao2026epigenetic,
title = {{Epigenetic Regulatory Networks in Cardiac Fibrosis: Therapeutic Targets, Crosstalk, and Future Directions.}},
author = {Yansheng Yao and Chongyu Shao and Haitong Wan},
journal = {Drug design, development and therapy},
year = {2026},
month = oct,
doi = {10.2147/dddt.s631934},
url = {https://europepmc.org/article/MED/42898927},
note = {CC BY-NC},
}
RIS
TY - JOUR
TI - Epigenetic Regulatory Networks in Cardiac Fibrosis: Therapeutic Targets, Crosstalk, and Future Directions.
AU - Yansheng Yao
AU - Chongyu Shao
AU - Haitong Wan
PY - 2026
DA - 2026/10/14
JO - Drug design, development and therapy
DO - 10.2147/dddt.s631934
UR - https://europepmc.org/article/MED/42898927
AB - Cardiac fibrosis is a central driver of pathological cardiac remodeling and a critical risk factor for the progression to heart failure. Cardiac fibrosis may induce myocardial ischemia and hypoxia, impaired cardiac function, and arrhythmias, and is thereby intimately linked to escalating cardiac mortality. Epigenetic mechanisms serve as core drivers in both the initiation and malignant evolution of cardiac fibrosis. Currently, the epigenetic regulatory network primarily covers five cutting-edge domains: (1) dynamic DNA methylation modifications, (2) the histone post-translational modifications, (3) emerging RNA epitranscriptomic modifications, (4) the non-coding RNA regulatory network, and (5) ATP-dependent chromatin remodeling. This review moves beyond conventional pathological frameworks to examine the multi-layered synergistic actions of epigenetic regulation in cardiac fibrosis. By deconstructing the specific spatiotemporal expression profiles of these dynamic modification mechanisms, we systematically evaluate their translational potential as reversible interventional targets, offering a critical synthesis of these epigenetic mechanisms and pointing to plausible research directions for overcoming fibrotic progression toward heart failure.
SN - 1177-8881
ER -