Mol Med Rep. 2026 Feb;33(2):66. doi: 10.3892/mmr.2025.13776. Epub 2025 Dec 12.
ABSTRACT
As the first functional organ to form during vertebrate embryogenesis, the heart exhibits heightened susceptibility to developmental toxicity. Epigenetic regulatory mechanisms, including DNA methylation, histone modifications, non‑coding RNAs, N6‑methyladenosine methylation and chromatin accessibility alterations, mediate cardiac developmental toxicity induced by exogenous compounds including environmental chemicals and pharmaceuticals. The present review comprehensively summarizes the current understanding of the molecular mechanisms through which these compounds exert cardiac developmental toxicity through epigenetic regulation. An in‑depth analysis of research progress and technical challenges across diverse epigenetic pathways is provided. By summarizing recent evidence, the present review proposes candidate epigenetic biomarkers for cardiac developmental toxicity monitoring and explores potential intervention strategies targeting these pathways. Future research should prioritize multi‑omics integration technologies and clinical translation system development. These advances are anticipated to foster innovation in both mechanistic research and preventive strategy development for cardiac developmental toxicity.
PMID:41384295 | DOI:10.3892/mmr.2025.13776