Abstract
During the early heart development, heart outflow tract elongates by the addition of cardiomyocytes from the anterior heart field (AHF)/secondary heart field (SHF). Dye-marking experiments in early chick embryos clarified that each AHF/SHF migrates to distinct conotruncal regions. Local administration of retinoic acid to the AHF/SHF causes distinct conotruncal heart defects in a region and stage dependent manner. For example, impaired development of AHF at HH stage 12 (corresponding to Carnegie stages 10–11 in human embryos) causes dextroposed aorta including transposition of the great arteries (TGA), while SHF at HH stage 12 persistent truncus arteriosus (PTA). Our results indicated that the abnormal development of certain AHF/SHF at certain stages causes specific spectrum of conotruncal heart defects.
Highlights
During the early heart development, heart outflow tract elongates by the addition of cardiomyocytes from the anterior heart field (AHF)/secondary heart field (SHF)
Developmental alterations of the heart outflow tract (OFT) cause conotruncal heart defects (CTHDs), which are often diagnosed in infants with congenital heart defects
Dye-marking experiments in chick embryos at the early looped-heart stage showed that the right and left AHFs migrate ipsilaterally to form the proximal OFT, whereas SHFs migrate rotationally to form the distal OFT beneath the semilunar valves [2]
Summary
During the early heart development, heart outflow tract elongates by the addition of cardiomyocytes from the anterior heart field (AHF)/secondary heart field (SHF). Keywords Second heart field · Heart outflow tract · Transposition of great arteries · Congenital heart defects · Retinoic acid Developmental alterations of the heart outflow tract (OFT) cause conotruncal heart defects (CTHDs), which are often diagnosed in infants with congenital heart defects.
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