<p>Polycystic ovarian syndrome (PCOS) has various etiologies, including insulin resistance (IR), hyperandrogenemia, and chronic low-grade inflammation. Cellular apoptosis sustains the dynamic equilibrium of biological processes. Physiological cell death is an active and programmed process essential for maintaining normal living functions. Pathological cell death is often induced by external injury or dysregulation of internal mechanisms, resulting in tissue dysfunction and disease. Numerous studies indicate that cells are activated by apoptosis, autophagy, pyroptosis, and ferroptosis in the context of oxidative stress, inflammation, and hyperandrogenemia, with these factors being closely linked to the pathophysiology of PCOS. This review summarizes the molecular mechanisms of cell death, including apoptosis, autophagy, and ferroptosis, and their effects on granulosa cells, oocytes, and theca cells. The pathways constitute a complex network of molecular interactions, providing new insights into the pathophysiology and therapeutic options for PCOS.</p>