HDP may affect the development of the respiratory system in offspring through a triple cascade mechanism: First, abnormal remodeling of the placenta-fetus interface signals, characterized by a significantly elevated ratio of soluble fms-like tyrosine kinase-1 (sFlt-1) to placental growth factor (PlGF) in preeclampsia, inhibits the vascular endothelial growth factor (VEGF) pathway, thereby impeding the maturation of alveolar type II epithelial cells. The gene discussed is FLT1; the disease is preeclampsia.