Follicular fluid-derived exosomal LncRNA LIPE-AS1 modulates steroid metabolism and survival of granulosa cells leading to oocyte maturation arrest in polycystic ovary syndrome.

The mammalian ovary is a unique organ that displays a distinctive feature of cyclic changes throughout the entire reproductive period. The estrous/menstrual cycles are associated with drastic functional and morphological rearrangements of ovarian tissue, including follicular development and degeneration, and the formation and subsequent atrophy of the corpus luteum. The flawless execution of these reiterative processes is impossible without the involvement of programmed cell death (PCD).PCD is crucial for efficient and careful clearance of excessive, depleted, or obsolete ovarian structures for ovarian cycling. Moreover, PCD facilitates selection of high-quality oocytes and formation of the ovarian reserve during embryonic and juvenile development. Disruption of PCD regulation can heavily impact the ovarian functions and is associated with various pathologies, from a moderate decrease in fertility to severe hormonal disturbance, complete loss of reproductive function, and tumorigenesis. This comprehensive review aims to provide updated information on the role of PCD in various processes occurring in normal and pathologic ovaries. Three major events of PCD in the ovary-progenitor germ cell depletion, follicular atresia, and corpus luteum degradation-are described, alongside the detailed information on molecular regulation of these processes, highlighting the contribution of apoptosis, autophagy, necroptosis, and ferroptosis. Ultimately, the current knowledge of PCD aberrations associated with pathologies, such as polycystic ovarian syndrome, premature ovarian insufficiency, and tumors of ovarian origin, is outlined.PCD is an essential element in ovarian development, functions and pathologies. A thorough understanding of molecular mechanisms regulating PCD events is required for future advances in the diagnosis and management of various disorders of the ovary and the female reproductive system in general. 

A matter of new life and cell death: programmed cell death in the mammalian ovary

Role of circular RNA/miRNA axes in the pathophysiology of polycystic ovary syndrome.

Polycystic Ovary Syndrome (PCOS) is a multifaceted endocrine disorder that implicates a spectrum of clinical manifestations, including hormonal imbalance, metabolic dysfunction, and even compromised ovarian granulosa cell (GC) activity. The underlying molecular mechanisms of PCOS remain elusive, presenting a significant barrier to effective diagnosis and treatment. This review delves into the emerging role of long non-coding RNAs (lncRNAs) in the pathophysiology of PCOS, articulating their intricate interactions with mRNAs, microRNAs, and other epigenetic regulators that collectively influence the hormonal and metabolic milieu of PCOS. We examine the dynamic regulatory networks orchestrated by lncRNAs that impact GC function, steroidogenesis, insulin resistance, and inflammatory pathways. By integrating findings from recent studies, we illuminate the potential of lncRNAs as biomarkers for PCOS and highlight their contribution to the disorder, offering a detailed perspective on the lncRNA-mediated modulation of gene expression and pathogenic pathways. Understanding targeted lncRNA interactions with PCOS proposes novel avenues for therapeutic intervention to ameliorate the reproductive and metabolic disturbances characteristic of the syndrome. 

Whispers of the Polycystic Ovary Syndrome Theater: Directing Role of Long Noncoding RNAs

The development and maturation of follicles are intricately linked to egg production and reproductive performance of chickens. Granulosa cells death directly affects the development and maturation of follicles, thereby impacting the reproductive performance of hens. Ferroptosis is a new type of cell death, it is unknown how it affects the growth and development of chicken follicles. In this study, RNA-seq analysis revealed significant differences in the expression of ferroptosis-related genes between normal follicles and atretic follicles, suggesting a potential role for ferroptosis in follicle growth and development. In addition, we found that ubiquitin-specific protease 13 (USP13) was significantly upregulated in atrophic follicles. Overexpression of USP13 results in depletion of glutathione (GSH), peroxidation of lipids, accumulation of iron, and activation of ferroptosis in chicken granulosa cells. In contrast, USP13 knockdown significantly inhibited ferroptosis events. Mechanistically, USP13 prevents the degradation of autophagy related 7 (ATG7) by deubiquitinating it, thereby enhancing the stability of ATG7 protein and ultimately promoting ferroptosis. In conclusion, this study elucidates the crucial role of the USP13-ATG7 axis in regulating ferroptosis in chicken follicle granulosa cells, thereby presenting a novel avenue for molecular breeding research in chickens.

USP13 regulates ferroptosis in chicken follicle granulosa cells by deubiquitinating ATG7

Background Numerous studies have suggested that ferroptosis plays a significant role in the development of polycystic ovary syndrome (PCOS), but the mechanism remains unclear. Methods In this study, we explored the role of ferroptosis-related genes in the pathogenesis of PCOS using a comprehensive bioinformatics method. First, we downloaded several Gene Expression Omnibus (GEO) datasets and combined them into a meta-GEO dataset. Differential expression analysis was performed to screen for significant ferroptosis-related genes between the normal and PCOS samples. The least absolute shrinkage selection operator regression and support vector machine–recursive feature elimination were used to select the best signs to construct a PCOS diagnostic model. Receiver operating characteristic curve analysis and decision curve analysis were applied to test the performance of the model. Finally, a ceRNA network-related ferroptosis gene was constructed. Results Five genes, namely, NOX1, ACVR1B, PHF21A, FTL, and GALNT14, were identified from 10 differentially expressed ferroptosis-related genes to construct a PCOS diagnostic model. Finally, a ceRNA network including 117 lncRNAs, 67 miRNAs, and five ferroptosis-related genes was constructed. Conclusion Our study identified five ferroptosis-related genes that may be involved in the pathogenesis of PCOS, which may provide a novel perspective for the clinical diagnosis and treatment of PCOS.

https://www.frontiersin.org/articles/10.3389/fmed.2023.1120693/pdf

Relationships of ferroptosis-related genes with the pathogenesis in polycystic ovary syndrome

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Relationships of ferroptosis-related genes with the pathogenesis in polycystic ovary syndrome