ArticleInternational journal of molecular sciences2019
Diabetic Pregnancy and Maternal High-Fat Diet Impair Mitochondrial Dynamism in the Developing Fetal Rat Heart by Sex-Specific Mechanisms.
Article in International journal of molecular sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 52 citations in OpenAlex.
- Effect of paternal resveratrol intake on mitochondria and telomere length in mouse embryos and offspring.The Journal of reproduction and development · 2026Article
- Mitochondrial Dysfunction: A Critical Link Between Maternal Diet and Offspring Metabolic Health.Biomolecules · 2026Review
- Mommy issues: how maternal diet shapes offspring mitochondrial physiology.Journal of animal science · 2026Review
- Maternal nutritional imbalance during pregnancy and the development of fetal-origin cardiovascular diseases.Frontiers in nutrition · 2026Review
- Maternal High-Fat Diet Worsens Necrotizing Enterocolitis via Effects on Mitochondrial Function in Newborn Mice.Cellular and molecular gastroenterology and hepatology · 2026Article
- DNMT1 promotes bladder cancer progression and immune escape by inhibiting MYH11 expression by methylating its promoter.International urology and nephrology · 2025Article
- Article
- The Transgenerational Impact of High-Fat Diet and Diabetic Pregnancy on Embryonic Transcriptomics and Mitochondrial Health.Biomedicines · 2025Article
- Mitochondrial ultrastructural pathology in diabetic cardiomyopathy: integrated analysis via scanning electron microscopy and 3D visualization imaging.Cardiovascular diabetology · 2025Article
- Piezo1 deletion mitigates diabetic cardiomyopathy by maintaining mitochondrial dynamics via ERK/Drp1 pathway.Cardiovascular diabetology · 2025Article
- Mitochondrial Dysfunction in Congenital Heart Disease.Journal of cardiovascular development and disease · 2025Review
- Research Progress of Mitochondrial Dynamics and Autophagy in Diabetic Complications: New Treatment Strategies.Diabetes, metabolic syndrome and obesity : targets and therapy · 2025Review
- NOTCH1 and UPR signaling in embryonic heart development under maternal high-fat diet influence.Frontiers in medicine · 2025Article
- Pregnancy in obese women and mechanisms of increased cardiovascular risk in offspring.European heart journal · 2024Review
- Early Methylglyoxal Exposure Leads to Worsened Cardiovascular Function in Young Rats.Nutrients · 2024Article
- Maternal androgen excess inhibits fetal cardiomyocytes proliferation through RB-mediated cell cycle arrest and induces cardiac hypertrophy in adulthood.Journal of endocrinological investigation · 2024Article
- Mitochondrial non-energetic function and embryonic cardiac development.Frontiers in cell and developmental biology · 2024Review
- Novel insights into the role of mitochondria in diabetic cardiomyopathy: molecular mechanisms and potential treatments.Cell stress & chaperones · 2023Review
- Research Progress of Maternal Metabolism on Cardiac Development and Function in Offspring.Nutrients · 2023Review
- Made in the Womb: Maternal Programming of Offspring Cardiovascular Function by an Obesogenic Womb.Metabolites · 2023Review
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Infants born to diabetic or obese mothers are at greater risk of heart disease at birth and throughout life, but prevention is hindered because underlying mechanisms remain poorly understood. Using a rat model, we showed that prenatal exposure to maternal diabetes and a high-fat diet caused diastolic and systolic dysfunction, myocardial lipid accumulation, decreased respiratory capacity, and oxidative stress in newborn offspring hearts. This study aimed to determine whether mitochondrial dynamism played a role. Using confocal live-cell imaging, we examined mitochondrial dynamics in neonatal rat cardiomyocytes (NRCM) from four prenatally exposed groups: controls, diabetes, high-fat diet, and combination exposed. Cardiac expression of dynamism-related genes and proteins were compared, and gender-specific differences were evaluated. Findings show that normal NRCM have highly dynamic mitochondria with a well-balanced number of fusion and fission events. Prenatal exposure to diabetes or a high-fat diet impaired dynamism resulting in shorter, wider mitochondria. Mechanisms of impaired dynamism were gender-specific and protein regulated. Females had higher expression of fusion proteins which may confer a cardioprotective effect. Prenatally exposed male hearts had post-translational modifications known to impair dynamism and influence mitophagy-mediated cell death. This study identifies mitochondrial fusion and fission proteins as targetable, pathogenic regulators of heart health in offspring exposed to excess circulating maternal fuels.
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