ArticleAmerican journal of physiology. Heart and circulatory physiology2026
Sex-dependent epigenomic and transcriptomic reprogramming links maternal obesity to cardiac remodeling in adult offspring.
Article in American journal of physiology. Heart and circulatory physiology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Maternal obesity during pregnancy predisposes the offspring to a high risk of developing cardiovascular and metabolic diseases later in life. This study investigated cardiac perturbations caused by maternal obesity by utilizing a mouse model of maternal high-fat diet (HFD)-induced obesity that recapitulates metabolic abnormalities observed in humans. Our study revealed that offspring of HFD-fed mothers (Off-HFD) exhibit a progression of obesity, dyslipidemia, and metabolic inflexibility when compared with offspring of regular diet-fed mothers (Off-RD). Deeper investigation of cardiac function revealed profound functional, metabolic, vascular, and immune perturbations in adult Off-HFD mice, with marked sex-specific differences. Although both male and female Off-HFD mice developed progressive cardiac hypertrophy, male offspring exhibited a more severe phenotype characterized by hypertension, increased vascular stiffness, cardiac dysfunction, and fibrosis. To identify potential mechanisms underlying these changes, we performed DNA methylation analysis in collected hearts of newly weaned and adult offspring. This analysis revealed extensive, sex-dependent alterations in DNA methylation within or nearby genes involved in cardiac development, lipid metabolism, hypertrophic growth, and inflammatory signaling. Importantly, many of these epigenetic alterations persisted into adulthood, suggesting that maternal obesity establishes a durable molecular memory in the offspring heart. Consistent with these findings, transcriptome analysis of adult hearts revealed activation of gene programs associated with heart failure and pathological cardiac remodeling in male Off-HFD mice, whereas female Off-HFD mice showed activation of pathways consistent with adaptive or cardioprotective responses. Together, these findings demonstrate that maternal HFD induces early-life epigenetic remodeling in the offspring heart that persists into adulthood and is associated with sex-specific metabolic, functional, vascular, and immune dysregulation. By linking early epigenomic changes to adult cardiac disease susceptibility, this study identifies potential developmental windows for preventive and early therapeutic interventions aimed at reducing cardiovascular risk in offspring exposed to maternal obesity in utero.
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