Abstract
Small for gestational age (SGA) infants affected by placental insufficiency are exposed to the risk of stillbirth and long-term complications. Based on RNA-seq and mass spectrometry, we identified dysregulated RNAs and proteins from the comparisons of SGA placental tissues and controls. We revealed two SGA-relevant co-expression modules (SRMs) that also significantly distinguished SGA from controls. Then we performed an integrated analysis of transcriptomic and proteomic profiles to trace their links to SGA as well as their significant correlations. For the core functional molecules we screened, we revealed their potential upstream regulators and validated them experimentally in an independent cohort. Overall, we pointed out insights into different molecular pathways for the pathological mechanisms of SGA and indicated potential target molecules that may be drivers of placental aberrations in the SGA infants.