The highs and lows of programmed cardiovascular disease by developmental hypoxia: studies in the chicken embryo

N Itani1,2, C E Salinas3, M Villena1

  • 1Department of Physiology, Development & Neuroscience, University of Cambridge, Downing Street, Cambridge, CB2 3EG, UK.

Insights

Adverse pregnancy conditions can program fetal cardiovascular dysfunction. The chicken embryo model isolates stressors like hypoxia, revealing their specific impacts on heart development and function.

Area of Science:

  • Developmental biology
  • Cardiovascular science
  • Environmental health

Background:

  • Adverse pregnancy conditions can lead to fetal origins of cardiovascular dysfunction.
  • Early life environmental stressors, including hypoxia, nutrition, and stress hormones, may promote offspring cardiovascular dysfunction.
  • Disentangling individual stressors in humans and mammals is challenging due to maternal/placental factors.

Purpose of the Study:

  • To review studies using the chicken embryo model to investigate isolated developmental stressors.
  • To determine the effects of chronic developmental hypoxia on prenatal growth, cardiovascular development, and pituitary-adrenal function.

Main Methods:

  • Utilizing the chicken embryo as a model to isolate effects of oxygenation, nutrition, or stress hormones.
  • Examining isolated chronic developmental hypoxia, independent of maternal physiology.
  • Summarizing studies on prenatal growth, cardiovascular development, and pituitary-adrenal function.

Main Results:

  • The chicken embryo model allows for the isolation of specific stressors on cardiovascular development.
  • Chronic developmental hypoxia has demonstrable effects on prenatal growth and cardiovascular development.
  • Isolated hypoxia impacts pituitary-adrenal function in the developing chicken embryo.

Conclusions:

  • The chicken embryo model is valuable for studying the independent effects of developmental stressors on cardiovascular programming.
  • Understanding isolated stressor impacts is crucial for comprehending fetal origins of cardiovascular disease.
  • Further research using this model can elucidate mechanisms of cardiovascular dysfunction programming.