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Early-life cardiovascular programming by maternal protein restriction: Electrophysiological, structural, and

Luísa C Gomes1, Matheus N Fioretto1, Lucas S Lemos1

  • 1Department of Cellular and Molecular Biology, Institute of Biosciences, Sao Paulo State University, Botucatu, SP, Brazil.

Experimental Cell Research
|July 5, 2026
PubMed
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Maternal protein restriction in rats leads to early heart changes in female offspring, including altered electrical activity and extracellular matrix remodeling. These findings highlight the impact of maternal nutrition on offspring cardiovascular health.

Area of Science:

  • Developmental Biology
  • Cardiovascular Physiology
  • Nutritional Science

Background:

  • Maternal malnutrition is a significant risk factor for adverse offspring health outcomes, particularly cardiovascular disorders.
  • The Developmental Origins of Health and Disease (DOHaD) concept posits that early life exposures can lead to long-term health consequences.
  • Maternal protein restriction (MPR) is a known experimental model linked to cardiovascular and hypertensive phenotypes in offspring.

Purpose of the Study:

  • To investigate the effects of maternal protein restriction (MPR) on the cardiovascular morphophysiology of female offspring at postnatal day 21 (PND21).

Main Methods:

  • Pregnant rats were assigned to a control (normoprotein) or gestational and lactational low-protein (GLLP) diet.
  • Female offspring were assessed at PND21 for electrocardiography, morphology, molecular changes, and oxidative stress.
Keywords:
Cardiac physiologyDOHaDEarly lifeMaternal malnutritionOxidative stress

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  • Analyses included heart weight, electrocardiogram (ECG) parameters, cardiomyocyte structure, extracellular matrix components, gene expression, and redox status.
  • Main Results:

    • GLLP offspring showed reduced body weight and length but increased relative heart weight, indicating disproportionate growth.
    • Electrocardiographic analysis revealed a shortened P-R interval and decreased heart rate in GLLP offspring.
    • Morphological analysis showed increased collagen and elastin deposition, suggesting early extracellular matrix remodeling.
    • Molecular analysis indicated reduced PRDX3 expression and altered antioxidant homeostasis (decreased CAT activity, GSH levels, and TBARS).

    Conclusions:

    • Maternal protein restriction induces early structural, molecular, oxidative, and electrophysiological alterations in the hearts of female offspring.
    • These adaptations may represent developmental programming events that increase susceptibility to cardiovascular dysfunction later in life.
    • The study underscores the critical role of maternal nutrition in programming long-term cardiovascular health across generations.