Key result
Epigenetic modifications, such as DNA methylation and histone changes, regulate the pathological crosstalk between cardiac fibroblasts and other cardiac cells during cardiovascular stress and injury.
Why the study?
Understanding cardiac mechanisms during injury and stress is needed, particularly how epigenetic mechanisms regulate cardiac fibroblasts and their crosstalk with other cardiac cell types.
Epigenetic regulation plays a crucial role in the pathological crosstalk between cardiac fibroblasts and other cardiac cells, offering potential novel therapeutic targets for cardiovascular diseases.
Cardiac fibroblast-ECM regulation and crosstalk may drive heart failure; leaves open targeted therapies pending prospective validation.
With the global impact of cardiovascular disease, there is a dire need to understand the mechanisms in the heart during injury and stress. It has been shown that the regulation of the extracellular matrix via cardiac fibroblasts plays a major role in the progression of heart failure and worsening function of the heart. Importantly, it has been suggested that crosstalk between other cardiac cells like cardiomyocytes, immune cells, and endothelial cells are influenced by the pathological function of the fibroblasts. This decline in function across all cardiac cells is seemingly irreversible. However, epigenetic mechanisms have been shown to regulate functionality across cardiac cells and improve outcomes during stress or injury. This epigenetic regulation has also been shown to control communication between different cell types and influence the role of multiple cardiac cell types during injury. The goal of this review is to summarize and discuss the current research of epigenetic regulation of cardiac fibroblasts and the subsequent crosstalk with other cardiac cell types in cardiovascular disease states.
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Kraus et al. (2025) conducted a review in Cardiovascular disease. Epigenetic regulation was evaluated. Epigenetic modifications, such as DNA methylation and histone changes, regulate the pathological crosstalk between cardiac fibroblasts and other cardiac cells during cardiovascular stress and injury.
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