The human placenta serves as the predominant endocrine organ throughout pregnancy, assuming a central role in preserving endocrine homeostasis, facilitating maternal physiological adaptation, and safeguarding fetal well-being. Preeclampsia (PE), a multifaceted and systemic gestational complication, stands a primary contributor to maternal and perinatal morbidity and mortality. Defective placental development has been extensively acknowledged as the fundamental pathological foundation underlying this condition. Accumulating evidence has unveiled a disruption in the balance of steroid hormone production within placentas affected by early-onset PE (E-PE). Considerable endeavors have been undertaken to decipher the endocrine mechanisms driving E-PE. Recent investigations have illuminated a complex, multi-tiered regulatory system that governs placental steroidogenesis, encompassing epigenetic controls such as microRNAs (miRNAs) activity and metabolic flux-conjugated histone acetylation, post-translational modifications including O-linked β-N-acetylglucosamine (O-GlcNAc), as well as intricate endocrine feedback loops among steroids and other signaling molecules like melatonin. Notably, a growing body of evidence robustly supports a causal link between elevated placental testosterone (T0) synthesis and the onset of PE. Nevertheless, comprehensive studies exploring the endocrine pathophysiology of PE remain essential to illuminate novel therapeutic avenues for mitigating this adverse pregnancy outcome.