Polycystic ovary syndrome (PCOS) is a complex and heterogeneous endocrine disorder affecting 5%-15% of women of reproductive age worldwide. It is characterized by hyperandrogenemia, ovulatory dysfunction, and polycystic ovarian morphology, and is associated with long-term risks of chronic conditions such as obesity, cardiovascular disease, and diabetes mellitus. Although the etiology of PCOS remains incompletely understood, the intricate interplay of genetic predisposition, environmental factors, and epigenetic modifications plays a pivotal role in its pathogenesis. ETS1 (E26 transformation specific 1), a transcription factor, is involved in regulating diverse critical biological processes, including cell proliferation, differentiation, angiogenesis, immune response, and apoptosis. Accumulating evidence suggests that ETS1 may play a significant role in the development and progression of PCOS, particularly in ovarian function, hyperandrogenesis, and inflammatory responses. This review aims to comprehensively summarize recent advances in understanding the role of ETS1 in the pathophysiological mechanisms underlying PCOS, elucidate its potential molecular mechanisms, and evaluate its potential as a therapeutic target for PCOS. The findings may provide insights into the etiology of PCOS and facilitate the development of novel therapeutic strategies.