Deciphering epigenetic regulation in cardiac developmental toxicity: Mechanisms and implications (Review)

Area of Science:

• Developmental toxicology
• Epigenetics
• Cardiovascular embryogenesis

Background:

• The heart, the first organ in vertebrate development, is vulnerable to toxic insults.
• Exogenous compounds (environmental chemicals, pharmaceuticals) can induce cardiac developmental toxicity.
• Epigenetic mechanisms are key mediators of this toxicity.

Purpose of the Study:

• To comprehensively review the molecular mechanisms of epigenetic regulation in cardiac developmental toxicity.
• To analyze research progress and technical challenges in epigenetic pathways.
• To propose epigenetic biomarkers and intervention strategies for cardiac developmental toxicity.

Main Methods:

• Literature review of studies on epigenetic regulation and cardiac developmental toxicity.
• Analysis of various epigenetic mechanisms: DNA methylation, histone modifications, non-coding RNAs, N6-methyladenosine methylation, and chromatin accessibility.
• Synthesis of current research findings and identification of knowledge gaps.

Main Results:

• Epigenetic modifications significantly influence how environmental compounds cause cardiac developmental toxicity.
• Diverse epigenetic pathways are involved, presenting complex research challenges.
• Candidate epigenetic biomarkers for monitoring toxicity and potential therapeutic targets were identified.

Conclusions:

• Epigenetic regulation plays a critical role in cardiac developmental toxicity.
• Further research integrating multi-omics and clinical translation is needed.
• Developing targeted interventions and biomarkers can improve prevention and management of cardiac developmental toxicity.