ArticleiScience2024
Maternal high-fat diet alters Tet-mediated epigenetic regulation during heart development.
Article in iScience, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
8 citing papers in PubMed.
- Sex-dependent epigenomic and transcriptomic reprogramming links maternal obesity to cardiac remodeling in adult offspring.American journal of physiology. Heart and circulatory physiology · 2026Article
- Butyrate counteracts maternal obesity-induced cardiac defects by promoting PLEKHG3-actin binding.EMBO reports · 2026Article
- Maternal-Fetal Crosstalk in Cardiovascular Programming: Linking the Intrauterine Environment to Lifelong Disease Risk.Journal of cardiovascular development and disease · 2026Review
- Epigenetic Perspectives on Maternal Gut Microbiota's Impact on Embryonic and Fetal Development.Comprehensive Physiology · 2026Review
- Article
- Maternal Nutritional Programming: Sex-Specific Cardiovascular and Immune Outcomes Following Perinatal High-Fat Diet Exposure.Nutrients · 2025Article
- The functional significance of vascular DNA hypermethylation in atherosclerosis: a historical perspective.Frontiers in pharmacology · 2025Review
- Review
Corrections and comments
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Authors and funding
7 authors.
Funding
Abstract
Imbalanced dietary intake, such as a high-fat diet (HFD) during pregnancy, has been associated with adverse offspring outcomes. Metabolic stress from imbalanced food intake alters the function of epigenetic regulators, resulting in abnormal transcriptional outputs in embryos to cause congenital disorders. We report herein that maternal HFD exposure causes metabolic changes in pregnant mice and non-compaction cardiomyopathy (NCC) in E15.5 embryos, accompanied by decreased 5-hydroxymethylcytosine (5hmC) levels and altered chromatin accessibility in embryonic heart tissues. Remarkably, maternal vitamin C supplementation mitigates these detrimental effects, likely by restoring iron, a cofactor for Tet enzymes, in a reduced state. Using a genetic approach, we further demonstrated that the cardioprotective benefits of vitamin C under HFD conditions are attributable to enhanced Tet activity. Our results highlight an interaction between maternal diet, specifically HFD or vitamin C, and epigenetic modifications during early heart development, emphasizing the importance of balanced maternal nutrition for healthy embryonic development.
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Registered trials
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