Polycystic Ovary Syndrome (PCOS) is a complex endocrine condition affecting women of reproductive age, characterized by hyperandrogenism, anovulation, and polycystic ovary morphology. It is influenced by environmental and genetic factors with high heritability and is associated with metabolic issues such as insulin resistance (IR), chronic inflammation, and oxidative stress. Despite extensive research, the molecular mechanism behind PCOS pathophysiology is still not fully understood. Recent studies highlighted the role of telomere biology and telomerase activity (TA), particularly that of telomere reverse transcriptase (TERT), in the development and progression of PCOS. Telomerase, a complex of ribonucleoprotein enzymes, is responsible for maintaining telomere length (TL). TERT promotes telomere stability, and its disturbance has been associated with reproductive diseases such as PCOS. This study critically examines the results of current studies on the TERT gene and its association with PCOS, as well as the mechanism underlying the reduction in TERT gene expression in women with PCOS. The review also highlights the key molecular discoveries related to TERT dysregulation in PCOS and its impact on clinical outcomes, suggesting that TERT expression levels can reflect disease severity, ovarian reserve, and the effectiveness of treatments in PCOS patients. TERT expression may be restored, and ovarian function may be enhanced by interventions focusing on oxidative damage, inflammation, or metabolic disorders. Future research may employ experimental methods such as telomerase activation, gene editing, and modification of TERT regulators. Elucidating the molecular mechanisms connecting TERT to ovarian dysfunction could enhance PCOS understanding and lead to the development of novel diagnostic markers and treatment strategies.
Balgote et al. (Fri,) studied this question.