Eduardo Retama Méndez

Epigenetic mechanisms have emerged as key regulators of acute myocardial infarction (AMI) pathophysiology, fine tuning gene expression without altering the underlying DNA sequence. Among these mechanisms, DNA methylation and histone modifications play pivotal roles in inflammation, apoptosis, angiogenesis, and tissue remodeling. During AMI and atherosclerosis, dysregulated expression of genes such as CREG, FOXP3, VEGF, BCL2, and NOS3 has been documented, driven by enzymes including DNMT3B and TET proteins. Likewise, histone methylation at residues H3K4, H3K9, and H3K27 modulates transcriptional activity in vascular cells under the control of enzymatic complexes such as EZH2 and G9a. This mini review analyses how these epigenetic mechanisms contribute to ischemic injury and highlight their relevance to the molecular understanding of AMI.

Congenital Heart Diseases (CHDs) are a heterogeneous group of structural abnormalities affecting the heart and major arteries, which are present in at least 1% of births worldwide. Studies have linked CHD to both genetic and environmental factors. In this regard, it has been demonstrated that changes in the epigenetic pattern impact the expression of key genes involved in proper cardiac development. Therefore, it is suggested that aberrant epigenetic mechanisms may contribute to the development of these pathologies. Here, we review and summarize the main epigenetic mechanisms involved in CHD. Moreover, cardiac development and the importance of the environment and CHD are also addressed.