MONDAY, Oct. 13 (HealthDay News) -- Healthy cells in an embryonic mouse heart can regenerate and replace diseased ones during development, but they may not be able to completely offset the later onset of cardiac problems, a new study shows.
The findings, previously observed only in non-mammals, give researchers insight into how early onset cardiac disease may occur in humans despite normal heart function early in life, scientists say.
The researchers at the University of Washington in Seattle genetically engineered embryonic female mice with hearts composed of half normal cells and half "diseased" cells that lacked mitochondria, a cell structure required for energy production. Mitochondria issues are a leading cause of fatal early onset cardiomyopathies, according to the researchers.
However, by the time the mice were born, only about 10 percent of the cardiac tissue was diseased, and the hearts were fully functional. However, more than 40 percent of the adult mice later developed premature cardiac disease.
"Our findings reveal an impressive regenerative capacity of the fetal heart that can compensate for an effective loss of half of the cardiac tissue," researcher Timothy C. Cox, a professor at the University of Washington, said in a school news release. "To the best of our knowledge, this represents the first in vivo demonstration of selection against diseased tissue during embryonic heart development."
The findings also led the researchers to theorize that healthy cell groups within the heart may be better able to regenerate themselves than diseased ones.
The study was published in the Oct. 14 issue of Developmental Cell.
The American Heart Association has more about heart disease.
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