ArticleMolecular metabolism2021
Maternal obesity persistently alters cardiac progenitor gene expression and programs adult-onset heart disease susceptibility.
Article in Molecular metabolism, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.
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Who cites it
11 citing papers in PubMed, 1 synthesis or guideline pooled it, 23 citations in OpenAlex.
- Maternal obesity and offspring cardiovascular remodelling - the effect of preconception and antenatal lifestyle interventions: a systematic review.International journal of obesity (2005) · 2024Pooled it
- Maternal obesity remodels nutrient transport transcriptional programs in early mouse embryonic and extraembryonic cell lineages.Molecular metabolism · 2026Article
- The Impact of Overweight and Obesity on Pregnancy: A Narrative Review of Physiological Consequences, Risks and Challenges in Prenatal Care, and Early Intervention Strategies.Current diabetes reports · 2025Review
- Lifelong high-fat, high-sucrose diet causes sex-specific heart dysfunction in mouse offspring.Academia medicine · 2025Article
- Pregnancy in obese women and mechanisms of increased cardiovascular risk in offspring.European heart journal · 2024Review
- Fetal programming and lactation: modulating gene expression in response to undernutrition during intrauterine life.Pediatric research · 2024Article
- Integrated small RNA, mRNA and protein omics reveal a miRNA network orchestrating metabolic maturation of the developing human heart.BMC genomics · 2023Article
- Research Progress of Maternal Metabolism on Cardiac Development and Function in Offspring.Nutrients · 2023Review
- KDM8 epigenetically controls cardiac metabolism to prevent initiation of dilated cardiomyopathy.Nature cardiovascular research · 2023Article
- Article
- Developmental toxicant exposures and sex-specific effects on epigenetic programming and cardiovascular health across generations.Environmental epigenetics · 2022Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
objectiveHeart disease risk can be programmed by intrauterine exposure to obesity. Dysregulating key transcription factors in cardiac progenitors can cause subsequent adult-onset heart disease. In this study, we investigated the transcriptional pathways that are altered in the embryonic heart and linked to heart disease risk in offspring exposed to obesity during pregnancy.
methodsFemale mice were fed an obesogenic diet and mated with males fed a control diet. Heart function and genome-wide gene expression were analyzed in adult offspring born to obese and lean mice at baseline and in response to stress. Cross-referencing with genes dysregulated genome-wide in cardiac progenitors from embryos of obese mice and human fetal hearts revealed the transcriptional events associated with adult-onset heart disease susceptibility.
resultsWe found that adult mice born to obese mothers develop mild heart dysfunction consistent with early stages of disease. Accordingly, hearts of these mice dysregulated genes controlling extracellular matrix remodeling, metabolism, and TGF-β signaling, known to control heart disease progression. These pathways were already dysregulated in cardiac progenitors in embryos of obese mice. Moreover, in response to cardiovascular stress, the heart of adults born to obese dams developed exacerbated myocardial remodeling and excessively activated regulators of cell-extracellular matrix interactions but failed to activate metabolic regulators. Expression of developmentally regulated genes was altered in cardiac progenitors of embryos of obese mice and human hearts of fetuses of obese donors. Accordingly, the levels of Nkx2-5, a key regulator of heart development, inversely correlated with maternal body weight in mice. Furthermore, Nkx2-5 target genes were dysregulated in cardiac progenitors and persistently in adult hearts born to obese mice and human hearts from pregnancies affected by obesity.
conclusionsObesity during pregnancy alters Nkx2-5-controlled transcription in differentiating cardiac progenitors and persistently in the adult heart, making the adult heart vulnerable to dysregulated stress responses.
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