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January 9, 2026Journal of the American Heart AssociationOpen Access

Maternal exercise did not reduce congenital heart defects in offspring of eNOS +/− mice with pregestational diabetes despite improving heart morphology.

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Key result

Maternal exercise did not reduce congenital heart defects in offspring of eNOS +/− mice with pregestational diabetes despite improving heart morphology.

Authors

RNRyleigh van NeckXLXiangru LuTPThomas Pan

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Overview

Investigates how endothelial nitric oxide synthase affects fetal heart development during maternal exercise in pregestational diabetes, suggesting key dependencies.

Key Points

  • To investigate the role of endothelial nitric oxide synthase (eNOS) in maternal exercise-mediated protection of fetal heart development in a pregestational diabetes (PGD) mouse model.
  • Induction of PGD in eNOS +/− and wild-type female mice
  • Exercise regimen via voluntary running wheels for pregnant females
  • Assessment of hearts at embryonic day 12.5 for proliferation, apoptosis, and oxidative stress
  • Analysis of fetal hearts collected at embryonic day 18.5 for congenital heart defects and eNOS protein levels
  • Maternal exercise improved litter size and reduced mortality in diabetic offspring of eNOS +/− females
  • CHD incidence remained unchanged in offspring of both wild-type and eNOS +/− females
  • Exercise increased coronary artery density without affecting capillary density
  • Proliferation deficits were restored by exercise, while oxidative stress was elevated
  • Maternal exercise did not alter eNOS protein or phosphorylation levels in fetal hearts

Cite This Study

Neck et al. (2025) studied this question. Maternal exercise did not reduce congenital heart defects in offspring of eNOS +/− mice with pregestational diabetes despite improving heart morphology.

synapsesocial.com/papers/69612fdc30ef6c21f6853e1ahttps://doi.org/10.1161/jaha.125.042848
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