Molecular Insights into Elevated Autoantibodies in Polycystic Ovary Syndrome: Mechanisms and Clinical Implications

Polycystic ovary syndrome (PCOS) is a prevalent endocrinological condition among women of reproductive age, characterized by several well-known symptoms, including hyperandrogenism, anovulation, irregular menstrual cycles, and insulin resistance. In addition, women suffering from PCOS are also at an increased risk of developing several autoimmune diseases, including thyroid disorders, type 1 diabetes, and rheumatoid arthritis. Furthermore, an elevated prevalence of diverse autoantibodies is observed in women diagnosed with PCOS. These include antibodies specific to autoimmune diseases, e.g., anti-thyroid peroxidase (anti-TPO), anti-thyroglobulin (anti-TG), and antinuclear antibodies (ANAs), as well as those that are non-specific, such as anti-malondialdehyde-modified human serum albumin (anti-HSA-MDA) or anti-α-crystallin. It appears that several mechanisms may be responsible for this phenomenon. PCOS has been observed to co-occur with autoimmune diseases, potentially attributable to shared genetic susceptibility or the presence of hormonal disorders resulting from autoimmune diseases. Moreover, PCOS is a chronic low-grade inflammatory disease that may contribute to immune dysfunction and subsequent overproduction of autoantibodies. A further intriguing aspect may be the yet-unknown role of autoantibodies in the pathogenesis of PCOS, considering PCOS as a disease with an autoimmune etiology.