Numerous histological studies have demonstrated that impaired placentation processes are involved in the key pathogenetic mechanisms of great obstetrical syndromes (GOSs). However, the molecular basis of this discovery is still unclear. Therefore, the objectives of this work were to characterize the molecular mechanisms and to search for new genetic markers of pregnancy complications via an integrative analysis of the data obtained by genome-wide expression profiling of placental tissue in preeclampsia, intrauterine growth restriction (IUGR), premature labor (PL), and physiological pregnancy (PP). Oxidative stress, ferroptosis, and disordered intercellular interactions in placenta were assumed to be common pathogenetic mechanisms of GOSs. A total of 64 genes were found to be significantly dysregulated in at least two pregnancy complications. Maternal endothelial cells and syncytiotrophoblast cells were the most significant cell populations enriched in these genes. A computational analysis and the topology of the protein-protein interaction network identified SOD1, ACTG1, TXNRD1, TKT, GCLM, GOT1, ACO1, and UBB as hub genes. A set of key regulators that trigger the reaction cascades involving the differentially expressed genes was found to include MAPK3, MID1, LCMT1, DUSP10, TOPS, SOX10, EGFR, TFAP2A, GLIS1, NR2F1, NR2F2, PAX5, HSF1, and BCL6. The genes were overrepresented in the MAP kinase and interferon-γ response signaling pathways. The above genes and their products were assumed to provide the most promising biomarkers for developing new approaches to risk factor assessment and targeted therapy in GOSs. Further studies should be aimed at clarifying their functional and diagnostic significance in pregnancy complications.