Abstract
Congenital Diaphragmatic Hernia (CDH) is a common birth defect associated with high mortality and severe respiratory deficiency in survivors. A general feature of CDH is the herniation of the abdominal tissues into the chest cavity, leading to malformation of the lung. The cellular and molecular mechanisms underlying CDH remain poorly understood. We found that mice deficient in the function of two Roundabout (Robo) receptors, Robo1 and Robo2, exhibit defects resembling CDH. Determination of the origin of these defects led to an unexpected role of Robo in the separation of foregut from the dorsal body wall, a morphogenetic process that is vital, yet rarely studied. Together, these data suggest for the first time that delayed separation of the foregut tissues from the dorsal body wall may contribute to the etiology of CDH in humans.
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