In utero exposure to maternal diabetes exacerbates dietary sodium intake-induced endothelial dysfunction by activating cyclooxygenase 2-derived prostanoids

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Abstract
Using a unique mouse model of prenatal exposure to maternal type 1 diabetes, our study demonstrates the novel observation that prenatal exposure to maternal diabetes results in a predisposition to high-salt (HS) dietary-induced vascular dysfunction and inflammation in adulthood. Mechanistically, we demonstrated that in utero exposure to maternal diabetes and HS intake induces vascular oxidative stress, cyclooxygenase-derived prostaglandin E2, and inflammation.
Funding Information
  • American Heart Association (CDA, 857268)
  • American Heart Association
  • Burroughs Wellcome Fund (Next Generation Pregnancy Initiative (1022517))
  • HHS | NIH | National Heart, Lung, and Blood Institute (HL14013903)
  • HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases (R01DK125015, R01DK137410)
  • RDCRN | Nephrotic Syndrome Study Network
  • São Paulo Research Foundation (2022/06639-2)
  • University of Pittsburgh (start-up funds)
  • NIDDK Diabetic Complications Consortium (RRID:SCR_001415)

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