Objective: To synthesize current evidence on mechanisms, diagnostic evaluation, and treatment of infertility in PCOS, with emphasis on phenotype-specific implications and integrative management.
Methods: A narrative review was conducted using PubMed, Scopus, and Web of Science from January 2015 to March 2024. Search terms included “PCOS,” “infertility,” “phenotype,” “letrozole,” “metformin,” “gonadotropins,” and “ART.” Eligible studies involved human females aged 18–45 years, written in English, and focused on PCOS-related infertility. Randomized trials, meta-analyses, and international guidelines were critically assessed for methodological rigor and clinical relevance.
Results: PCOS accounts for 70–80% of anovulatory infertility, with marked variability across phenotypes. Phenotype A, combining hyperandrogenism, ovulatory dysfunction, and polycystic ovarian morphology, carries the greatest reproductive and metabolic burden. Biomarkers such as AMH, testosterone, DHEAS, fasting insulin, and HOMA-IR improve risk stratification. Lifestyle modification restores ovulation in up to 60% of overweight patients. Letrozole is superior to clomiphene, while gonadotropins and ART are effective in resistant cases. Metformin enhances ovulatory and pregnancy outcomes in insulin-resistant women. IVF protocols using antagonists and agonist triggers improve safety by reducing ovarian hyperstimulation syndrome. Psychological comorbidities, particularly anxiety and depression, are frequent and negatively affect fertility outcomes.
Conclusion: PCOS-related infertility requires a personalized, multidisciplinary approach. Integration of phenotype-based assessment, biomarker evaluation, lifestyle intervention, and tailored reproductive strategies optimizes outcomes. Addressing metabolic and psychological dimensions further improves reproductive success and long-term health.
Tag Archives: polycystic ovary syndrome
Identification and expression of microRNA-34a-3p and its target Rapamycin-insensitive companion of mTOR (RICTOR) in polycystic ovarian syndrome in South Indian population
Objectives: Polycystic Ovarian Syndrome (PCOS) is a complex condition affecting 4% to 26% of the world-wide population and is characterized by enlarged ovaries and cysts. These cysts are actually immature ovarian follicles that have failed to mature and release an egg, which is a process known as anovulation. This study aims to explore the potential of miRNA as therapeutic and diagnostic biomarkers for PCOS, focusing on the identification and expression analysis of novel candidates like miR-34a-3p and its target Rapamycin-insensitive companion of mTOR (RICTOR). The objective is to enhance our understanding of the molecular mechanisms associated with PCOS, particularly the roles of miRNAs in its pathogenesis. In future, we plan to test miR-34a-3p mimics/inhibitors and RICTOR downregulation to improve insulin sensitivity and ovarian function. We will also explore combined therapies and conduct trials to assess their efficacy and safety in PCOS patients, aiming to develop practical treatments for PCOS.
Methods: National Centre for Biotechnology Information (NCBI) database, TargetScan, and miRbase were explored to identify the novel miRNA candidates, resulting in the discovery of miR-34a-3p. Secondary structure was constructed using RNA Fold, and Ct and melt curve analysis assessed its statistical expression levels. Additionally, similar research was conducted to analyze the expression levels of RICTOR, a target of miR-34a-3p.
Result: The secondary structure showed miR-34a-3p has a minimum free energy of -47.20 kcal. Additionally shows dysregulation in both miR-34a-3p and RICTOR in individuals with PCOS. Furthermore, overexpression of RICTOR and decrease in miR-34a-3p levels suggest their possible role in the pathogenesis of PCOS.
Conclusion: In PCOS, miR-34a-3p is downregulated, and there’s an inverse relationship between miR-34a-3p and RICTOR levels. qRT-PCR results showed high RICTOR expression in PCOS patients. RICTOR plays a crucial role in the mTOR pathway, affecting insulin signaling, metabolism, and cellular growth, which are all implicated in PCOS.