An overview of the placenta's role in the development of congenital diaphragmatic hernia

TL;DR

This paper reviews how the placenta may contribute to the development of congenital diaphragmatic hernia, focusing on molecular pathways and placental abnormalities.

Contribution

The paper introduces the novel perspective of placental involvement in CDH pathogenesis, which has not been previously explored.

Findings

The placenta's role in CDH is suggested through its connection to fetal development and molecular pathways like retinoic acid.

Evidence from animal and human studies indicates a complex interplay between placental function and CDH.

Further research on placental contributions may lead to improved diagnostics and therapies for CDH.

Abstract

Congenital diaphragmatic hernia (CDH) is a severe congenital malformation resulting from incomplete diaphragm development, leading to abdominal organ herniation into the thoracic cavity. This disruption compromises pulmonary development, frequently resulting in lung hypoplasia and pulmonary hypertension. While the role of the placenta in congenital heart defects is well established, its involvement in congenital lung diseases, particularly CDH, remains unexplored. During the prenatal period, the placenta serves as a crucial site for nutrient and gas exchange between the mother and the fetus, and given its functional connection to fetal development, it provides a compelling avenue for investigating the pathophysiology of CDH. This review synthesizes current knowledge regarding the placental contribution to CDH, with a focus on molecular pathways, particularly the retinoic acid pathway and placental abnormalities. Evidence from both animal models and human studies suggests a complex interplay between placental function and CDH pathogenesis. Further investigation is required to elucidate the placenta's role in disease mechanisms, which may offer perspectives for future research, advances in prenatal diagnostics, and therapeutic strategies.

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