The research has come from the Victor Chang Cardiac Research Institute, in the U.S. the focus is on how cellular stress affected congenital defects of the heart, plus other organs like the kidneys.
A congenital heart defect is a problem in the structure of the heart that is present at birth. Symptoms can vary from none to life-threatening and can be manifest as rapid breathing, bluish skin, poor weight gain, and feeling tired. The associated complications include heart defects and can lead to heart failure.
Some cases of the congenital diseases are genetic; however, as the new research points out, many are related to environmental circumstances. To explore the impact of environmental factors, the research group studied how short-term oxygen deficiency altered the course of heart development in mouse embryos.
The mouse embryos were exposed to oxygen levels that were as low as 5.5 percent for a period of eight hours. The reduced levels of oxygen coincided with damage to the developing hearts. The patterns of damage mirrored those seen with humans.
It is thought that the reduced oxygen triggers a stress response in embryonic heart cells. The cells respond by stopping protein production, and that loss of proteins leads to malformed heart developing.
Other forms of cellular stress may trigger a similar response. The stress triggers could include viral infections, elevated temperature, high blood glucose, nutritional problems or wider environmental pollution. In addition, these stresses may affect other organs. This represents an area for further research.
Speaking with Laboratory Roots, the lead researcher, Professor Sally Dunwoodie, said: “We obviously know that smoking is terrible for an unborn baby’s health. But oxygen deficiency in an embryo can be caused by many things, for example prescription medications, high blood pressure, high altitude, a tangled umbilical cord, as well as carbon monoxide.”
The findings are published in the journal Development. The research paper is headed “Gestational stress induces the unfolded protein response, resulting in heart defects.”
