Background/Objectives: The role of the endometrial microbiome in reproductive failure remains incompletely understood. This study aimed to describe the composition of the endometrial microbiome in women evaluated for infertility or recurrent miscarriage. Methods: In this single-center descriptive study, endometrial samples were collected from women evaluated for infertility or recurrent miscarriage. Microbiome profiling was performed using 16S rRNA gene next-generation sequencing. Samples were classified as Lactobacillus-dominant when Lactobacillus spp. accounted for ≥90% of the total bacterial community. Alpha diversity was assessed using the Shannon and Simpson indices, while beta diversity was evaluated using Bray-Curtis dissimilarity, principal coordinates analysis (PCoA), PERMANOVA, and PERMDISP. Results: Of the 60 samples, 20 (33.3%) were Lactobacillus-dominant and 40 (66.7%) were non-Lactobacillus-dominant. Across all samples, Firmicutes was the predominant phylum (76.6%). Non-Lactobacillus-dominant samples showed significantly higher alpha diversity than Lactobacillus-dominant samples for both the Shannon and Simpson indices (p = 1.19 × 10-6 and p = 1.51 × 10-6, respectively), as well as higher observed taxa richness (p = 0.000017). PCoA based on Bray-Curtis dissimilarity demonstrated clear separation between microbiome profiles, supported by PERMANOVA (pseudo-F = 13.87, R2 = 0.193, p = 0.001). PERMDISP showed significantly greater dispersion among non-Lactobacillus-dominant samples (F = 566.94, p < 0.001). Non-Lactobacillus-dominant samples showed greater representation of Enterococcus and Prevotella. Conclusions: In this cohort non-Lactobacillus-dominant communities were more frequent with greater diversity, richness, and compositional heterogeneity than Lactobacillus-dominant communities. These findings highlight the need for larger, standardized studies with appropriate control populations to clarify their clinical significance.

Background/Objectives: Traditional semen analysis techniques frequently result in incorrect male infertility diagnoses, despite advancements in assisted reproductive technology (ART). Reduced fertilization potential, decreased embryo development, and lower pregnancy success rates are associated with elevated DNA Fragmentation Index (DFI), which has been proposed as a diagnostic indicator of sperm DNA integrity. Improving reproductive outcomes requires incorporating DFI into predictive models due to its diagnostic importance. Methods: In this study, semen samples were stratified into low and high DFI groups across two datasets: the “Reference” dataset (162 samples) containing sperm motility (A, B, and C), total sperm count, and morphology percentage, and the “ORP” dataset (37 samples) with the same features plus oxidation-reduction potential (ORP). We trained and evaluated four machine learning (ML) models—Logistic Regression, Support Vector Machines (SVM), Bernoulli Naive Bayes (BNB), and Random Forest (RF)- using three feature subsets and three preprocessing techniques (Robust Scaling, Min-Max Scaling, and Standard Scaling). Results: Feature subset selection had a significant impact on model performance, with the full feature set (X_all) yielding the best results, and the combination of Robust and MinMax scaling forming the most effective preprocessing pipeline. Conclusions: ORP proved to be a critical feature, enhancing model generalization and prediction performance. These findings suggest that data enrichment, particularly with ORP, could enable the development of ML frameworks that improve prognostic precision and patient outcomes in ART.

Adipocytes produce the hormone leptin, a hormone that links energy availability to reproductive function by permitting activation of the hypothalamic-pituitary-gonadal (HPG) axis. Loss-of-function mutations in the long leptin receptor isoform (LEPRb) disrupt intracellular signaling pathways, including the Janus kinase 2 (JAK2)/signal transducer and activator of transcription 3 (STAT3), phosphoinositide 3-kinase (PI3K), and mitogen-activated protein kinase (MAPK) pathways, resulting in central leptin resistance and impaired neuroendocrine control of reproduction. Evidence from human monogenic obesity syndromes, animal models, and neuroendocrine studies indicates that LEPRb mutations disrupt hypothalamic circuitry upstream of gonadotropin-releasing hormone (GnRH) neurons, impairing GnRH pulsatility and leading to hypogonadotropic hypogonadism (HH) and infertility. This review synthesizes molecular, translational, and clinical data highlighting the central role of kisspeptin-mediated signaling in leptin-dependent reproductive regulation. Current therapeutic limitations are discussed alongside emerging approaches, including kisspeptin-based therapies and receptor-targeted strategies. Elucidating how LEPRb dysfunction disrupts metabolic-reproductive integration may provide insights into both rare monogenic conditions and common obesity-associated reproductive dysfunction.

Conventional semen analysis frequently fails to identify the underlying pathophysiology of male infertility, which is a complicated clinical disease, especially in cases of idiopathic infertility. A growing body of research indicates that inflammation and oxidative stress (OS) are important and related factors in male reproductive failure. Excessive reactive oxygen species (ROS) promote lipid peroxidation, protein oxidation, mitochondrial dysfunction, and sperm DNA fragmentation, thereby compromising motility, morphology, and fertilizing capacity. Concurrently, pro-inflammatory mediators like interleukin-6 (IL-6), interleukin-8 (IL-8), and tumor necrosis factor-alpha (TNF-α) are frequently found in the seminal plasma of infertile men and are linked to poor semen parameters and testicular dysfunction. It is crucial that oxidative and inflammatory pathways work together to create a self-sustaining pathophysiological cycle that exacerbates sperm damage and destabilizes the reproductive milieu. The diagnostic significance, clinical suitability, and limitations of oxidative stress and inflammation biomarkers, such as malondialdehyde (MDA), 8-hydroxy-2′-deoxyguanosine (8-OHdG), total antioxidant capacity (TAC), and specific inflammatory markers, are critically assessed in this comprehensive review. The lack of established diagnostic thresholds, methodological variation, and translational issues that still restrict their widespread clinical implementation are highlighted in particular. Additionally, the potential contribution of biomarker-guided approaches to focused therapy decisions and individualized patient management is explored. This study examines how oxidative and inflammatory markers may complement conventional male infertility assessments by supporting more precise, mechanism-based approaches in reproductive medicine, while addressing diagnostic readiness and translational limitations.

Background and Objectives: The microbiome plays a pivotal role in male infertility, with distinct microbial species exerting both beneficial and deleterious effects on reproductive function. Sexually transmitted bacteria and several viruses, including human papillomavirus (HPV), have been identified in semen. This cross-sectional study aimed to examine the prevalence of single and co-infections of sexually transmitted bacteria (STB)-such as Chlamydia trachomatis, Mycoplasma spp., and Ureaplasma spp.-with various HPV subtypes in Greek male partners of infertile couples and to evaluate their potential impact on sperm parameters. In addition, the possible effect of cryopreservation on the maintenance of these pathogens was assessed. Materials and Methods: Eighty-two semen samples were initially collected from 82 individuals undergoing routine sperm analysis. In total, 80/82 (97.6%) participants proceeded to further analysis, as 2/82 (2.4%) were excluded due to poor DNA quality. Results: A total of 18/80 (22.5%) sperm samples tested positive for STB, with Ureaplasma spp. representing the most frequently detected pathogen. Co-infection of Ureaplasma spp. and Mycoplasma hominis was observed in 4/80 (5%) samples. Twelve samples (12/80, 15%) were positive for HPV, including low-risk (LR) and high-risk (HR) types, and HPV 16 was the predominant HR genotype. Notably, a co-infection of STB and HPV was not found in our specimens. STB-positive samples demonstrated significantly higher sperm concentration and improved progressive motility compared with STB-negative samples. HPV-positive samples exhibited lower sperm volume and concentration and increased non-progressive motility compared with HPV-negative samples. Following three months of cryopreservation, LR HPV and STB were no longer detectable, whereas HR HPV types remained detectable. Conclusions: These preliminary findings are interesting, as they could be useful for routine screening of HPV and STB in sperm samples preserved in sperm banks and highlight the need for future research.

A significant and persistent issue in assisted reproduction is recurrent implantation failure (RIF), which is often observed even after the transfer of embryos of high morphological and/or genetic quality. Accumulating data suggest that exposure to chemicals with endocrine-disrupting effects (EDCs) may be associated with adverse implantation outcomes. Many environmentally widespread substances have the potential to interfere with the regulation of the endocrine system, affecting critical mechanisms involved in implantation, such as endometrial receptivity, steroid hormone receptor signaling, immune tolerance at the maternal–fetal interface, and the epigenetic regulation of genes that are essential for successful implantation. Experimental studies have shown that exposure to EDCs can alter gene expression in the endometrium, inflammatory pathways, and the dynamics of early embryonic development, while clinical and epidemiological data have associated increased levels of EDCs in the body with lower implantation rates in assisted reproductive technology (ART) cycles. This narrative review examines the implications of these findings in reproductive medicine, summarizes recent experimental and clinical data, and highlights the molecular mechanisms linking exposure to endocrine disruptors with recurrent implantation failure. Recognizing environmental chemical exposure as a potentially modifiable risk factor may offer new perspectives for the prevention of RIF and the development of more personalized therapeutic strategies.

Bisphenols, phthalates, and other plastic-associated compounds are endocrine-disrupting chemicals (EDCs), common environmental contaminants that can disrupt hormonal homeostasis. Human exposure to such chemicals occurs mainly through food packaging, consumer goods, medical devices, and the environment, starting right from early development stages up to adulthood. These chemicals might cause damage to male reproductive systems as a result of being anti-androgens and estrogenic chemicals. However, the proper development of the male reproductive system requires well-regulated hormonal signaling pathways; hence, exposure to such compounds during the developmental stages poses a great risk. Environmental exposure to plastics during fetal development may influence the development of the testes, reduce the function of the Leydig cells, disrupt steroidogenesis, and produce epigenetic modifications, as documented through studies. This has been shown to increase the risk of developing reproductive disorders and reduce the production of testosterone. Therefore, one of the pathophysiological links between endocrine disruptor exposure and ED might be testosterone deficiency. Apart from disrupting testosterone production, the plastic-sourced EDCs could influence various physiological processes associated with erectile performance, such as those related to vasculature, inflammation, metabolism, and endocrinology. In this review, a comprehensive overview of the scientific data on the effect of plastic-based EDCs on testosterone regulation and male reproductive health has been provided. The role of developmental programming, endocrine disruption, oxidative stress, epigenetics, and vascular dysfunction has been explored in detail. Moreover, the possible involvement of micro- and nanoplastics has also been reviewed. From the data that is currently available, there seems to be a physiologically plausible association between plastic-based contaminants, testosterone dysregulation, and adverse reproductive outcomes.

The hallmark feature of empty follicle syndrome (EFS) is failure to retrieve oocytes from apparently mature follicles despite adequate ovarian stimulation and appropriate ovulation triggering. Although considered uncommon, with a reported prevalence ranging from 0.2% to 7%, EFS may have a profound clinical and psychological impact and can recur in assisted reproductive technology (ART) cycles. Modern classification systems divide EFS into genuine and false forms. Genuine EFS is potentially associated with intrinsic abnormalities involving luteinizing hormone/choriogonadotropin receptor (LHCGR) signaling, oocyte competence, and cumulus–oocyte interaction, whereas false EFS is primarily attributed to pharmacokinetic or pharmacodynamic factors resulting in inadequate trigger exposure. Borderline EFS represents a third phenotype characterized by incomplete or partial impairment of final oocyte maturation. This review examines the pharmacodynamics of ovulation-triggering agents, including human chorionic gonadotropin (hCG), gonadotropin-releasing hormone (GnRH) agonist protocols, and dual-trigger strategies, and their roles in regulating final oocyte maturation. The molecular aspects of periovulatory signal transduction and the mechanisms of LHCGR activation, epidermal growth factor (EGF)-like pathways, and meiotic resumption in relation to EFS etiopathogenesis will be described. The impact of patient-dependent conditions like obesity, poor ovarian reserve, polycystic ovary syndrome (PCOS), and pituitary response on trigger response will be assessed. New approaches like post-trigger monitoring of hormones and rescue treatment with gonadotropins represent a valuable method for avoiding cycle cancellation in patients at risk. Overall, EFS is increasingly regarded not as a single disorder but as a heterogeneous spectrum of periovulatory dysfunction arising from pharmacological, endocrine, and intrinsic ovarian factors that impair completion of final oocyte maturation.

Crucial regulators of gamete metabolism and signaling, mitochondria synchronize energy generation with redox equilibrium and developmental proficiency. Once thought of as hazardous byproducts, reactive oxygen species (ROS) are now understood to be vital signaling molecules that provide a “redox window of competence” that is required for oocyte maturation, sperm capacitation, and early embryo development. This review presents the idea of mitochondrial metabolic checkpoints, which are phases that govern gamete quality and fertilization potential by interacting with cellular signaling, redox balance, and mitochondrial activity. Recent research shows that oocytes may sustain a nearly ROS-free metabolic state by blocking specific respiratory-chain components, highlighting the importance of mitochondrial remodeling in gamete competence. Evidence from in vitro and in vivo studies shows that ROS act as dynamic gatekeepers at critical points in oogenesis, spermatogenesis, fertilization, and early embryogenesis. However, assisted reproductive technologies (ARTs) may inadvertently disrupt this redox–metabolic equilibrium. Potential translational benefits can be obtained via targeted techniques that optimize mitochondrial function, such as modifying oxygen tension, employing mitochondria-directed antioxidants like MitoQ and SS-31, and supplementing with nutraceuticals like melatonin, CoQ10, and resveratrol. Understanding ROS-mediated checkpoints forms the basis for developing biomarkers of gamete competence and precision therapies to improve ART outcomes. By highlighting mitochondria as both metabolic sensors and redox regulators, this review links fundamental mitochondrial biology to clinical reproductive medicine.

Spinal cord injury is strongly associated with male infertility, traditionally attributed to erectile and ejaculatory dysfunction. However, accumulating evidence demonstrates that infertility in this population extends beyond neurogenic impairment and involves profound biochemical and molecular alterations within the male reproductive system. The objective of this review is to synthesize current evidence on the role of oxidative stress, inflammation, and sperm DNA damage as central mechanisms driving impaired fertility in men with spinal cord injury. A comprehensive evaluation of clinical and experimental studies indicates that seminal plasma in affected individuals is characterized by elevated reactive oxygen species, reduced antioxidant capacity, and a pro-inflammatory cytokine profile, including increased levels of tumor necrosis factor alpha, interleukin 6, and interleukin 1 beta. These alterations are closely linked to leukocytospermia, mitochondrial dysfunction, and disruption of the blood-testis barrier, creating a toxic microenvironment that compromises sperm function. As a consequence, spermatozoa exhibit reduced motility, impaired membrane integrity, and significantly increased DNA fragmentation and chromatin abnormalities. Elevated sperm DNA damage has been consistently associated with poor fertilization outcomes, reduced embryo quality, and increased risk of pregnancy loss in assisted reproductive settings. Importantly, these molecular defects persist even when sperm are retrieved using advanced techniques such as electroejaculation or surgical extraction, highlighting the need for targeted therapeutic strategies. Interventions aimed at reducing oxidative stress and modulating inflammation, including antioxidant supplementation and advanced sperm selection methods, show promise but remain insufficiently standardized. Future research should focus on the development of personalized approaches integrating molecular diagnostics and targeted therapies to improve reproductive outcomes in this population. Collectively, this review reframes spinal cord injury-related infertility as a complex inflammatory and oxidative disorder and underscores the importance of addressing sperm DNA integrity in clinical management.

Background/Objectives: Hypogonadotropic hypogonadism (HH) is an uncommon but treatable cause of non-obstructive azoospermia (NOA). Fertility can often be restored with gonadotropin therapy. This study evaluated spermatogenic and reproductive outcomes in men with HH-related NOA managed by stepwise gonadotropin therapy, microdissection testicular sperm extraction (microTESE) for persistent azoospermia, and assisted reproduction when indicated. Methods: A retrospective cohort study included 35 men treated between 2010 and 2022. Human chorionic gonadotropin (hCG), with or without follicle-stimulating hormone (FSH), was administered to induce spermatogenesis. Outcomes included sperm appearance in the ejaculate, microTESE sperm retrieval rate in persistent azoospermia, and pregnancy and live birth outcomes after natural conception or in vitro fertilization with intracytoplasmic sperm injection (IVF-ICSI) when required. Results: Mean gonadotropin therapy duration was 12.0 months (range 6-24). Sperm appeared in the ejaculate in 27/35 men (77%). The remaining 8/35 (23%) underwent microTESE, with sperm retrieved in 7/8 (88%). Seven couples proceeded to IVF-ICSI, undergoing 11 cycles that yielded 6 clinical pregnancies (55% per cycle) and 5 live birth deliveries, including 2 twin pregnancies. Among responders, 13 natural pregnancies occurred, resulting in 13 live birth deliveries, including 2 twin pregnancies. Overall, 18/35 men (51%) achieved biological fatherhood, corresponding to 18 live birth delivery events (4 twin and 14 singleton deliveries) and 22 newborns. Conclusions: In men with HH-related NOA, exogenous gonadotropin therapy is expected to induce spermatogenesis in most patients. MicroTESE provides high sperm retrieval rates for those without ejaculatory sperm. Through an integrated approach of hormonal induction, microsurgical sperm retrieval, and assisted reproduction, approximately half of patients may ultimately achieve biological fatherhood in longer-term follow-up, depending on baseline severity and partner factors.

BACKGROUND:Despite significant advances in genetics, immunology, and endometrial research, the underlying cause of nearly half of recurrent pregnancy loss (RPL) cases remains unknown. This highlights the limitations of conventional diagnostic approaches and underscores the need for methods that can detect complex, subtle biological patterns. OBJECTIVES:To summarize and critically assess how artificial intelligence (AI) is changing our knowledge of, ability to predict, and future therapeutic management of RPL, with a focus on machine learning (ML) approaches that identify latent biological pathways and multifactorial contributors to pregnancy loss. METHODS:This narrative review summarizes contemporary research on AI applications in reproductive medicine. Research using imaging, proteomic, genomic, clinical, and multi-omics information to create predictive or mechanistic models associated with RPL provided evidence. RESULTS:AI-based approaches are increasingly demonstrating the ability to detect complex interactions among environmental, immunological, biochemical, and genetic factors associated with RPL. ML and deep learning (DL) models enhance prognostic accuracy, identify novel candidate biomarkers, and provide insights into the systemic and molecular mechanisms underlying pregnancy loss. Integrating heterogeneous data through AI supports the development of personalized reproductive profiles and can improve prediction and counseling. CONCLUSIONS:AI has the potential to improve both personalized prediction and mechanistic understanding of RPL. However, clinical translation is currently hampered by a number of important issues, including small and diverse datasets, conflicting diagnostic definitions, limited external validation, and a lack of prospective clinical trials. To responsibly integrate AI tools into reproductive care, these limitations must be addressed.

Cellular senescence, mitochondrial dysfunction, and cumulative oxidative stress (OS) are the main causes of the progressive decreases in oocyte and sperm quality that define reproductive age. There is growing evidence that these processes are controlled by systemic variables, such as metabolites produced from the gut microbiome and extracellular vesicle (EV)-mediated intercellular communication, rather than being exclusively regulated at the tissue level. Antioxidant enzymes, regulatory microRNAs, and bioactive lipids that regulate mitochondrial redox balance, mitophagy, and inflammatory signaling are transported by EVs derived from reproductive organs, stem cells, immune cells, and the gut microbiota. Concurrently, microbiome-derived metabolites such as urolithin A, short-chain fatty acids, and polyphenol derivatives enhance mitochondrial quality control, activate antioxidant pathways, and suppress senescence-associated secretory phenotypes. This narrative review integrates the most recent research on the relationship between redox homeostasis, mitochondrial function, gut microbiota activity, and EV signaling in the context of male and female reproductive aging. We propose an emerging gut-EV-mitochondria axis as a unified framework through which systemic metabolic and antioxidant signals affect gamete competence, reproductive tissue function, and fertility longevity. Finally, we discuss therapeutic implications, including microbiome modulation, EV-based interventions, and senotherapeutic strategies, highlighting key knowledge gaps and future research directions necessary for clinical translation.

Although assisted reproductive technologies have significantly advanced the treatment of infertility, overall success rates remain limited by the lack of accurate and safe tools for assessing reproductive potential. Conventional embryo selection and endometrial evaluation rely largely on morphological and non-functional criteria, which provide only indirect insight into the underlying biological competence of the embryo oocyte and uterine environment. In this context the development of non-invasive biomarkers has emerged as a critical objective in modern reproductive medicine. This review discusses current evidence on non-invasive biomarkers in in vitro fertilization and assisted reproductive technologies with emphasis on embryo derived follicular fluid and endometrial indicators. Advances in time lapse imaging analysis of spent embryo culture media follicular fluid profiling and uterine fluid assessment are discussed in relation to their biological significance and association with clinical outcomes. The role of metabolomic proteomic transcriptomic and genetic signals is examined alongside emerging applications of artificial intelligence for data integration and outcome prediction. While numerous non-invasive biomarkers demonstrate promising associations with embryo viability implantation potential and surrogate pregnancy outcomes, with limited evidence in live birth rates, their clinical translation is constrained by methodological heterogeneity, limited validation, and challenges in standardization. Integrative multi parameter approaches rather than single biomarker strategies appear most likely to enhance predictive accuracy. Continued efforts toward data harmonization, large scale validation, and clinically oriented model development are essential for the successful incorporation of non-invasive biomarkers into routine IVF practice. Curated databases and relevant AI applications may facilitate and help progress non-invasive biomarkers in ART.

Background: This case–control study investigates whether miR-27a rs895819 A>G polymorphism is associated with an increased risk of recurrent pregnancy loss (RPL) in Caucasian Greek women. Methods: This study included 93 women with at least two unexplained miscarriages before the 24th week of gestation (RPL group) and 107 women with no pregnancy loss history (control group). The miR-27a rs895819 A>G polymorphism was detected using PCR amplification, followed by DraIII-HF restriction enzyme digestion. Results: The GG genotype was linked to a significantly higher risk of RPL (p-value = 0.00005), whereas the AA genotype was associated with a significantly lower risk (p-value = 0.00036). The AG genotype appeared more frequently in women with RPL (49.5% vs. 44.9% in controls), but the difference was not statistically significant (p-value = 0.5139). Conclusions: To our knowledge, this is the first study demonstrating that the miR-27a A>G polymorphism was significantly associated with a higher risk of recurrent miscarriage in Caucasian women. These findings provide evidence that the GG genotype may serve as a potential genetic marker for identifying women at higher risk of recurrent miscarriage, offering valuable insights for genetic counseling and reproductive medicine.

Female sexual dysfunction (FSD) is prevalent among women with multiple sclerosis (MS), leading to significant impairments in quality of life. Despite various available treatments, current approaches often fail to address the complex, multifactorial nature of FSD in this population. Transcutaneous tibial nerve stimulation (TTNS) has recently gained attention as a non-invasive neuromodulation therapy that has demonstrated potential benefits for neurogenic bladder dysfunction, with preliminary evidence suggesting overlapping improvements in sexual function. This narrative review synthesizes current evidence on the use of TTNS for managing FSD in women with MS. A comprehensive literature search of Medline, Web of Science, and Scopus was conducted, focusing on studies that explored TTNS interventions and outcomes in MS-related FSD. The findings indicate that TTNS likely modulates pelvic neural pathways, enhances genital blood flow, and improves key sexual function domains, including arousal, lubrication, and orgasm. Clinical studies using validated assessment tools, such as the Female Sexual Function Index (FSFI), have shown significant improvements in sexual outcomes, particularly when TTNS is combined with pelvic floor muscle training (PFMT). Experimental models further support the plausibility of these findings, linking TTNS to increased pelvic perfusion and more balanced neurogenic regulation of sexual response. Although initial evidence suggests that TTNS is safe, effective, and well-tolerated, limitations include small sample sizes, short follow-up periods, and variability in treatment protocols. Future research should focus on larger controlled trials, long-term follow-up studies, and standardized intervention parameters to optimize the application of TTNS for addressing FSD in women with MS.

This case presents a rare form of an ectopic pregnancy after retrograde migration of the transferred blastocyst to the fallopian tube. The presence of hydrosalpinx and extremely advanced maternal age further increases the risk. This case highlights the possibility of blastocyst migration even after ultrasound guidance during embryo transfer.

Background/Objectives: Infertility in both men and women can be significantly influenced by oxidative stress (OS), which occurs due to an imbalance between reactive oxygen species (ROS) and the body’s antioxidant defenses. In women, OS disrupts oocyte maturation, implantation, and the viability of the embryo; in men, it impairs sperm quality, reduces motility, and damages DNA integrity. This review explores existing research on how dietary and lifestyle interventions can reduce OS and enhance reproductive health outcomes. Methods: We conducted a comprehensive review of clinical, translational, and molecular studies exploring the mechanisms by which OS affects fertility, as well as the efficacy of nutritional and behavioral strategies. The interventions evaluated include weight management, regular exercise, micronutrient supplementation, antioxidant-rich diets, smoking and alcohol cessation, and stress-reduction techniques. Results: Specific dietary components such as zinc, selenium, vitamins C and E, and polyphenols have been found to neutralize reactive oxygen species (ROS) and enhance gamete function. OS is additionally reduced through lifestyle modifications, including minimizing harmful exposures, managing stress, and participating in moderate physical activity. Biomarkers such as ROS levels, total antioxidant capacity, 8-OHdG, and DNA fragmentation index are essential for assessing the effectiveness of interventions. Conclusions: Fertility in both sexes can be improved, and oxidative stress significantly reduced, through a multimodal approach incorporating dietary and lifestyle changes. There are encouraging opportunities to improve reproductive health through customized approaches that are informed by biomarker profiles. To incorporate these treatments into regular fertility care, future studies should concentrate on standardized procedures and long-term results.

Chronic inflammation is increasingly recognized as a critical factor in female reproductive health; influencing natural conception and the outcomes of assisted reproductive technologies such as in vitro fertilization (IVF). An essential component of innate immunity, the NLR family pyrin domain-containing 3 (NLRP3) inflammasome is one of the major mediators of inflammatory responses, and its activation is closely linked to oxidative stress. This interaction contributes to a decline in oocyte quality, reduced fertilization potential, and impaired embryo development. In the ovarian milieu, oxidative stress and NLRP3 inflammasome activation interact intricately, and their combined effects on oocyte competence and reproductive outcomes are significant. The aims of this review are to examine these molecular mechanisms and to explore therapeutic strategies targeting oxidative stress and NLRP3 inflammasome activity, with the goal of enhancing female fertility and improving clinical outcomes in reproductive health.

Background/Objectives: Cumulus cells have been proposed to be indicators of oocyte quality. In this study, oocyte cumulus cells were analyzed for SERPINE gene expression. High SERPINE gene expression in cumulus cells is associated with reduced oocyte maturity. However, high mRNA levels in granulosa cells are associated with follicles that result in pregnancy. This study aimed to evaluate SERPINE gene expression in cumulus cells across different ovarian stimulation protocols and its potential impact on follicle number, oocyte maturity, and embryo quality. Methods: The sample of the study consisted of 93 infertile women that underwent a five-day fixed antagonist protocol. Detection of SERPINE gene expression levels in cumulus cells was performed by extracting and isolating the total RNA produced in granulosa cells, and conducting cDNA synthesis and Real-Time Polymerase Chain Reaction. Results: The SERPINE gene expression in CCs was assessed in 71 samples. The SERPINE gene expression levels in CCs were categorized based on the ΔCp values. Most participants (65.9%) exhibited a high expression of the SERPINE gene, with ΔCp values greater than 2. Higher gene expression resulted in a higher number of follicles. However, no statistically significant results were observed regarding the number of follicles and the number of embryos. Conclusions: The study results provide insights into the expression patterns of the SERPINE gene in CCs and underscore the complexity of fertility-related biomarkers and the need for further investigation. SERPINE expression appears to be associated with follicle count, while its role in predicting oocyte quality and pregnancy success remains inconclusive.