Polycystic ovary syndrome (PCOS) has an endocrine pathophysiology that needs immediate clinical attention for effective mitigation, as a significant portion of the reproductive population is affected globally. Current treatment options for PCOS are symptom-specific, and more extensive research is imperative to meet the therapeutic needs of the disease. Besides studies, the assessment of novel anti-PCOS drugs can be more effectively carried out through experimentation, for which the choice of appropriate animal models based on parameters and pathways to be evaluated is crucial. For a good preclinical evaluation, the animal model must ensure disease reproducibility and predictive validity. The present review provides insights into the animal models reported in the literature for PCOS studies and the aspects in which various therapeutics under study can be evaluated using these models. These animal models are also classified based on the mode of induction, duration essential for induction, and species. Besides, mammalian, non-mammalian and transgenic models are also included. This review will provide a detailed analysis to the researchers working in the domain of PCOS to facilitate an easy choice of appropriate animal model for their study and to identify the scope of developing newer animal models for PCOS study.

Indiscriminate use of polystyrene (PS) plastics has posed a major problem for its disposal and recycling on one hand, while on the other hand, fragmentation of these into micro/nano compounds threatens the living world by its toxic effect. The small sized particles can be present in any ecosystem and pose threat to the living world there. The unique properties of these small-scale fragments allow them to cross the barriers of human bodies and affect the vital organ system, altering the normal physiological parameters. Male reproductive system is highly affected by these micro/nanoplastics which leads to infertility and other physiological complications. Smaller number of literatures has been reported in this field in comparison to female reproductive system. The signaling mechanism of polystyrene micro/nanoplastics (PSMP/NPs) have been discussed in this review. There are lacunae in this regard which have been addressed very specifically. Many reports of biodegradation processes have been put forward, but not without any additional hazards. This review puts together the existing literature on the effect of PSMP/NPs on mammalian male reproductive system, throws light on the possible bioremediation methods using microorganisms, and highlights the unattended areas of study so that the future research finds a way for these problematic aspects.

Polycystic Ovary Syndrome (PCOS) is a complex endocrine disorder affecting numerous women of reproductive age, characterized by a variety of clinical and biochemical features. Accurate classification and diagnosis of PCOS remains challenging due to the heterogeneous nature of its manifestations. This study introduces a robust machine learning framework that combines a voting ensemble model with two distinct feature selection techniques, Sequential Forward Selection (SFS) and Boruta, to enhance the accuracy in classifying PCOS. We also utilized Explainable Artificial Intelligence (XAI) techniques, such as Shapley Additive Explanations (SHAP), Local Interpretable Model-agnostic Explanations (LIME), Partial Dependence Plot (PDP), AnchorTabular, and Permutation Importance, to interpret the ensemble model. These methods provide essential insights into the significance of key features for predicting PCOS patients. Results show that the proposed ensemble learning model achieved optimal performance with the feature selection technique used. Specifically, the proposed voting ensemble classifier and features picked by SFS had the highest accuracy among all models. This method can help in PCOS diagnosis and support early intervention.

Advancements in the management of male infertility, particularly azoospermia, have significantly improved with the evolution of testicular biopsy techniques. This review explores the clinical applications and outcomes of three primary methods: testicular sperm aspiration (TESA), testicular sperm extraction (TESE), and microdissection TESE (mTESE). TESA remains a practical, minimally invasive solution for obstructive azoospermia, offering high success rates. However, its limited effectiveness in non-obstructive azoospermia (NOA) highlights the need for more refined approaches. mTESE has emerged as the preferred method in NOA cases due to its microsurgical precision, higher sperm retrieval rates, and reduced damage to testicular tissue. Multiple factors influence the success of these procedures, including patient age, testicular volume, hormone levels, and underlying histopathology. The identification of reliable predictive biomarkers such as follicle-stimulating hormone (FSH), inhibin B, anti-Müllerian hormone (AMH), and TEX101 has enhanced patient selection and procedural planning. Additionally, imaging techniques and metabolite profiling are emerging as valuable non-invasive tools for predicting outcomes. The integration of AI and machine learning into clinical practice further supports individualized treatment strategies by improving predictive accuracy and intraoperative decision-making. Despite clinical success, ethical and psychosocial considerations remain central to the comprehensive care of affected individuals. Financial constraints and unequal access to specialized reproductive services also pose challenges. Future efforts should prioritize the development of validated predictive models, the expansion of biomarker research, and the implementation of standardized clinical protocols. A multidisciplinary, patient-centered approach will be essential in optimizing outcomes for men facing infertility due to azoospermia.

Advancements in next generation sequencing technologies, including 16S rRNA amplicon sequencing, have vastly expanded our understanding of reproductive microbiota and its role in fertility. For example, in humans, the bacterial genus of is the overwhelmingly dominant commensal bacterium within reproductive tissues and fluids, such as the vagina, and is an indicator of fertility in women. Shifts away from allow for opportunistic pathogenic bacteria to inhabit the reproductive tract and result in dysbiosis and infertility. The goal of this review is to explore human reproductive microbiota including bacteria that commensally inhabit reproductive tissues and fluids as well as opportunistic pathogenic bacteria that can result in dysbiosis, infertility, and disease. Continued exploration of the microbiome and its association with reproductive health will aid in the development of targeted therapeutic strategies to positively modulate bacteria and improve fertility.

Male infertility accounts for approximately half of all infertility cases and is often linked to chromosomal abnormalities. While numerical and structural rearrangements are well recognized, the clinical significance of chromosomal polymorphisms remains unclear. To characterize the spectrum of cytogenetic alterations - including polymorphisms, structural rearrangements, and numerical changes - in men presenting with infertility and to assess their incidence on men with semen abnormalities. In this retrospective observational study, peripheral blood samples from 62 patients with detected cytogenetic alterations were collected at Genos Laboratory (Unimed Diagnostic Center) in Bauru, Brazil, between January 2015 and June 2020. Semen analysis reports for these patients were retrieved from the Fertility Clinic in Bauru, Brazil. Following specialist evaluation, a final cohort of 38 men diagnosed with infertility was analyzed. Results: Chromosomal polymorphisms were the most frequent alteration (77.4%), followed by structural rearrangements (17.7%) and numerical changes (4.8%). Among polymorphism carriers, 58% exhibited at least one abnormal semen parameter, most commonly asthenozoospermia (42%), teratozoospermia (38%), and oligozoospermia (33%). The 46,XYqh variant predominated (50%), with half of these cases demonstrating semen abnormalities. Double polymorphisms (46,XY9qh and 46,XY22ps;  = 8) were uniformly associated with oligozoospermia and teratozoospermia. Structural alterations - pericentric inversion of chromosome 9 and Robertsonian translocation rob(13;14)(q10q10) - were found in 11 patients; 72% of these also had semen abnormalities. Numerical alterations were rare but associated with abnormal semen parameters in 66% of cases. Chromosomal polymorphisms, though traditionally viewed as benign, were frequently detected in compromised semen quality in this cohort. Structural and numerical rearrangements, while less common, were detected in a higher proportion of abnormal semen parameters. These findings underscore the value of comprehensive cytogenetic screening in the evaluation of male infertility.

The placenta develops as a transient organ during pregnancy to nurture the growing fetus. It supplies nutrients and oxygen to the fetus, collects fetal waste, and safeguards the fetus from infections and adverse pregnancy conditions. Emerging evidence suggests that the placenta plays adaptive functions to protect the developing brain from injury in adverse maternal conditions. Inadequate placental support can impact the developmental process of the brain, which increases the risk of brain diseases among the offspring. There is a remarkable coordination in gene expression between the placenta and fetal brain of mice, suggesting a robust regulation of the brain-placental axis. The deregulation of the brain-placental axis can have adverse effects on the fetal programming of brain development. Defective neuronal development of the fetus due to the abnormal or non-optimal placental functions can lead to an increased risk of different neuropsychiatric diseases in the adult life of the offspring. Thus, there is a growing interest to understand placental influences on fetal brain development and its links to the risk of brain diseases. Research on the brain-placental axis, also referred to as neuroplacentology, is a rapidly emerging interdisciplinary field that integrates concepts and tools from diverse areas, including reproductive biology, neuroscience, epigenetics, systems biology, and data sciences, among others. Recently, large-scale multiomics data and systems biology approaches have been applied to investigate the functional links between the placenta and fetal brain, and to dissect the cellular and molecular mechanisms of the regulation of the brain-placental axis. The primary objective of this review is to outline the current status and the future avenues of this emerging research field that holds huge potential to advance our knowledge about the role of the placenta in the developmental origin of brain health and disease.

Human fetal development requires sustenance the placenta, which mediates molecular transport between maternal and fetal circulations. Placental formation begins as cells of the trophoblast lineage differentiate and the extraembryonic mesoderm becomes vascularized, assembling a unique organ that facilitates nutrient and gas exchange, waste removal, hormone production and immune modulation. We describe how placentation is orchestrated to keep pace with fetal growth, but is vulnerable to disruption by medical interventions for infertility. Initially, trophoblast stem cells differentiate into proliferating mononuclear cytotrophoblasts (CTBs) that fuse to form the multinucleated syncytiotrophoblast (STB). The STB ensheathes the chorionic villi, bathed in maternal blood. As fetal blood vessels develop within the mesodermal core of villi, the maternal-fetal interface is established. Where the villi meet the decidua, CTBs further differentiate into extravillous trophoblasts, which invade and remodel uterine arteries into high-conductance, low-resistance vessels, enhancing maternal blood flow to the placenta. Among the critical intercellular axes that govern trophoblast differentiation, invasion, and vascular remodeling hormonal cues, particularly those associated with the corpus luteum, are critical; their alteration in certain assisted reproductive technology (ART) protocols can contribute to incomplete arterial remodeling. Malplacentation is linked to miscarriage, fetal growth restriction, and preeclampsia, affecting over 10% of pregnancies, and occurring at higher rates in patients diagnosed with infertility, especially those who conceive through ART. Understanding the mechanisms driving these pathologies is essential for improving pregnancy outcomes. Strategies to optimize ART protocols and therapeutic interventions targeting key signaling pathways offer potential avenues to mitigate risks associated with malplacentation.

The embryonic aneuploidy in mammals may arise from impaired Spindle Assembly Checkpoint (SAC) function, a mechanism which prevents errors in chromosome segregation by blocking anaphase in response to spindle anomalies. Mammalian oocytes are particularly susceptible to these errors, possibly because the large oocyte volume favors dilution of the checkpoint signal, preventing its efficient function. This study aimed to investigate hypothesis that oocyte cytoplasmic volume affects SAC functionality. Oocyte size was manipulated in prophase oocytes (before nuclear envelope breakdown, NEBD) or in M-phase oocytes (after NEBD) by either reducing or increasing cytoplasmic volume by half. These oocytes were then cultured in the presence of nocodazole which activated the SAC by arresting oocytes in metaphase I of the first meiotic division. The functionality of SAC was assessed by measuring the proportion of oocytes escaping SAC-induced metaphase I arrest and completing the first meiotic division i.e., extruding the first polar body and entering the metaphase II of the second meiotic division. Reduction of the cytoplasmic volume in the prophase stage resulted in stronger checkpoint function, with only 4% of oocytes escaping SAC arrest compared to 36% of control normal-sized oocytes. Conversely, enlarged oocytes showed diminished checkpoint efficiency, with 54% bypassing checkpoint-induced arrest compared to 20% of control normal-sized oocytes. Importantly, no such relationship was observed when cytoplasmic volume was altered in oocytes after NEBD. This may suggest that the SAC depends on some nucleus-associated factors that are released into the cytoplasm after NEBD, since such factors would be twice as concentrated in oocytes undergoing volume reduction before NEBD compared to those undergoing reduction after NEBD. These results prove that SAC efficiency in mouse oocytes is influenced by cytoplasmic volume, with larger volumes impairing its function.

Components of the renin-angiotensin system (RAS) are expressed in both female and male reproductive tracts, with angiotensin I converting enzyme (ACE) being an important component for male reproductive function, as shown in animal models. The most studied polymorphism is the Alu insertion-deletion (I/D), which has been proposed to have a negative effect on male fertility. Given the conflicting evidence in the literature, we conducted a multicentric case-control study to investigate the association between the Alu I/D polymorphism and impaired spermatogenesis. Using PCR amplification and agarose electrophoresis, we genotyped the gene Alu I/D polymorphism in 745 South Slavic men. The study group consisted of 457 patients with impaired spermatogenesis, 239 with non-obstructive azoospermia (NOA) and 218 with oligoasthenoteratozoospermia (OAT) and a control group of 288 fertile men. No association was found between the Alu I/D polymorphism and these semen phenotypes, suggesting that it is not associated with NOA or severe OAT in this cohort. To provide a broader regulatory context, we also developed an integrative atlas of regulatory elements by in silico multi-omics analysis using genomics databases and bioinformatics tools. Data integration revealed various regulatory mechanisms at multiple omics levels, including genomics, epigenomics, miRNAomics, transcriptomics, proteomics and epiproteomics. These include genomic variants with predicted deleterious effects, a CpG island, microRNAs (miRNAs) and post-translational modifications (PTMs). In addition, protein interaction analysis revealed that ACE is indirectly linked to several proteins previously associated with male infertility and is also targeted by miRNA previously associated with oligozoospermia. This comprehensive, multi-faceted approach, combining genetic association analysis with bioinformatics, provides insights into regulation in its broader molecular context. These results emphasize the importance of further integrative multi-omics and systems biology research to better understand the role of ACE in male reproductive function.

In recent years, the incidence of male infertility has increased to approximately 10%, with a continued upward trend. Therefore, understanding the mechanisms underlying male infertility and developing effective treatment strategies have become essential areas of focus. Mitochondria are regulated by a complex quality control system including mitochondrial dynamics, mitophagy and biogenesis, which not only maintains mitochondrial structural and functional integrity, but also supports the stability of testicular tissue and the intracellular environment necessary for male fertility. Several studies have demonstrated that dysfunction in mitochondrial dynamics and mitophagy is closely associated with a decline in male fertility. Disruptions caused by excessive external stimuli or gene mutations can impair these processes, resulting in oxidative damage, apoptosis, inflammation, and ferroptosis. These pathological changes ultimately damage testicular cells and tissues. Consequently, this review will focus on the two key mechanisms: mitochondrial dynamics and mitophagy. Furthermore, mitochondrial biogenesis-responsible for producing new mitochondria and regulating the number of mitochondria-also plays an important role in maintaining male fertility. Related studies have shown that mitochondrial biogenesis dysfunction can trigger a cascade of pathological events that lead to testicular tissue damage. In summary, this review systematically examines the roles of mitochondrial dynamics and mitophagy in regulating male fertility. It provides an in-depth analysis of the pathological mechanisms by which dysfunction in these processes leads to male infertility. Additionally, this review summarizes current therapeutic agents targeting mitochondrial dynamics and mitophagy, aiming to identify potential strategies for the clinical treatment of male infertility.

The role of sperm morphology in male fertilization potential remains unclear. This study aimed to evaluate the incidence of specific sperm morphological abnormalities in a cohort of Turkish men attending a single-center infertility clinic and to assess their associations with semen quality and sperm functionality. A total of 2,923 men aged 17-57 years were included in this cross-sectional study. Semen parameters and specific morphological abnormalities in the head, neck-midpiece, tail, and cytoplasmic residue were analyzed according to WHO criteria. Participants were categorized into normal and low semen parameter groups based on sperm count, motility, and normal morphology. Associations between semen parameters and morphological abnormalities were assessed using Spearman correlation and binary logistic regression analyses. Head defects were the most prevalent abnormalities, followed by tail, neck-midpiece, and cytoplasmic residue. Normal sperm morphology and specific abnormalities were significantly associated with semen quality, with normal forms demonstrating the strongest predictive potential. Head defects were primarily associated with teratozoospermia, whereas neck-midpiece and tail defects were linked to motility impairments. Notably, round and tapered heads, bent necks, and coiled or short tails showed the strongest associations with progressive and rapid progressive motility, which are critical determinants of fertilization capacity. Our findings indicate that different categories of sperm abnormalities have distinct predictive potentials for semen quality disorders and suggest that specific defects may arise from disruptions in different stages of sperm morphogenesis.

Chronic prostatitis (CP) imposes a considerable global disease burden, with notable regional disparities in China and significant associated healthcare costs. Traditional classification systems, particularly type III subtypes, are hindered by high symptom heterogeneity and low treatment response rates. Recent advances in multi-omics approaches have elucidated the molecular mechanisms underlying CP, including genomic and epigenetic regulation, transcriptomic and immune microenvironment interactions, metabolomic and microbiome interplay, as well as proteomic and neural remodeling. Precision diagnostic techniques are evolving, integrating multi-omics biomarkers, imaging, and functional assessments for molecular subtyping and clinical translation. Targeted therapeutic strategies are emerging, focusing on immune microenvironment modulation, neuro-immune cross-intervention, and microbiome modulation. However, challenges in clinical translation remain, including technical bottlenecks in integrating dynamic multi-omics data and limitations of animal models. To address these issues, complementary strategies between real-world evidence and traditional randomized controlled trials are proposed. Looking forward, future directions include the development of AI-driven multimodal high-precision diagnostic systems and innovative combination therapies involving targeted, immunotherapeutic, and neuro-stimulatory approaches.

Early embryo development and competence mechanisms are paramount to ART's success but are still underexplored in human-relevant animal models. Clinical embryo evaluation remains largely based on subjectively evaluated morphological characteristics. In the current era of biomarkers and low-input high-throughput technologies, it is possible to investigate the multi-complex molecular landscape of the embryo during development from the zygote up to the blastocyst stage. The scope of this article is to review the underlying molecular mechanisms of pre-implantation embryo development. In addition, we briefly explore the latest advances in embryo quality assessment - including molecular and epigenetic evaluation and technical advances such as time-lapse imaging and artificial intelligence - together with clinical challenges for selecting the best embryo for single embryo transfer.

Assisted reproductive technologies (ART) have been widely and successfully used in both humans and livestock. However, only in humans and cattle have fertilization (IVF), embryo culture (IVC), and embryo transfer (ET) developed into large commercial sectors. The major differences between human and animal ART include the rationale of the treatment and the patient groups. While ART is used to treat infertility in humans, veterinary ART aims to maximize genetic gain and minimize generation intervals. Human ART is filled with societal, cultural, and emotional challenges, whereas veterinary ART aims to optimize economic success. While human ART deals with selected patients, including older individuals, veterinary ART focuses on young animals and a wide variety of species with different reproductive traits. Both human and veterinary ART face the shared challenge of establishing reliable tools to assess sperm fertilizing ability, evaluate oocyte developmental capacity, and support early embryo-maternal communication, which is pivotal for successful pregnancy. A holistic approach and comprehensive understanding of the underlying mechanisms and technologies across species could provide valuable insights for increasing ART success rates in both humans and animals.

Ovarian stimulation is applied to women undergoing IVF treatment with the aim of selecting more than one follicle. Until a few years ago, fresh embryo transfer was the norm, but not without the risk of ovarian hyperstimulation syndrome (OHSS). In recent years, vitrification has allowed the successful freezing of all oocytes or embryos, thus favoring multiple embryo transfer in subsequent thawing cycles and eliminating the risk of OHSS. Certainly, excess embryos from fresh embryo transfer cycles can be also frozen and thawed in future transfers. In terms of the number of oocytes needed, research in recent years has shown differences between fresh embryo transfer cycles and elective freezing of all embryos, termed elective freeze-all cycles, with the fresh cycle requiring an optimal number to avoid OHSS, while in elective freeze-all cycles there appear to be no specific upper limit. Consequently, the approach to ovarian stimulation may also differ between the two types of cycles. Although GnRH antagonists are used in both cycles, in elective freezing cycles progestins tend to replace antagonists in preventing the endogenous LH surge. However, it is unclear whether prevention of the LH surge is required in such cycles, since luteinization affecting the endometrium is not clinically relevant, as no embryo transfer occurs. This narrative review describes the current experience in ovarian stimulation for IVF, highlighting the differences between fresh and elective freeze-all cycles and the potentially different approach.

According to the World Health Organization (WHO), infertility is the failure of a couple to achieve pregnancy after one year of consistent unprotected sex. Male factors contribute to about 50 percent of all infertility cases. Male infertility is a multifactorial disease that can stem from multiple etiologies which can be congenital or acquired. Due to the complex nature of male infertility, a multifaceted approach is crucial for the diagnosis and treatment of the condition. But, in most cases, the cause of infertility is idiopathic. The diagnosis and management of male infertility is a comprehensive and stepwise process that involves history, physical examinations, and semen analyses which is the gold standard for evaluating male fertility in the clinic. The outcomes of semen analyses will determine the next step of investigation which may include hormone profiling, imaging, and genetic testing to identify the mechanism of infertility. Through advances in fertility research, Assisted Reproductive Technology has revolutionized the treatment approach for male infertility. ARTs like IVF and Intracytoplasmic sperm Injection have been useful in helping couples achieve pregnancy when all other treatment options have failed. Despite advances in fertility research, there are still challenges to be overcome such as improved access to fertility care, optimization of ART to achieve 100 percent clinical pregnancy, deeper understanding of etiologies of male infertility with emphasis on idiopathic male infertility. This review summarizes current knowledge on the etiologies, diagnosis, and therapeutic interventions as well as recent advances in basic and clinical research on male infertility.

This comprehensive review reflects our current knowledge of viral infections in the context of assisted reproduction, highlighting the latest research and guidelines. It focuses on the major viral pathogens that have a significant impact on human reproduction. It examines their impact on both male and female reproductive systems, fertility outcomes, and pregnancy, with a particular emphasis on managing the risks of transmission in assisted reproductive technologies (ART). State-of-the-art screening protocols and preventive measures are outlined, highlighting the progress made in minimizing viral transmission and ensuring safe reproductive outcomes. By presenting the current landscape of viral management in reproductive health, this review underscores the need for continued vigilance, research, and innovation to face viral threats.

The variation in reproductive age among individuals is significant, with many cases of infertility involving premature ovarian aging. This issue, combined with the societal trend of delaying childbearing, leads to age-related ovarian dysfunction. Ovarian aging is related to a decline of ovarian reserve, as oocyte quantity, quality, and precocious senescence, and may affect fertility and the overall individual well-being. Mitochondria play a central role in the maintenance of any cell health. Then mitochondrial dysfunctions may be responsible also for a negative impact on the quality, number, and function of oocytes, leading to different age-related reproductive disorders, impaired oogenesis, and embryogenesis. Although a large number of researches have shown clearly that mitochondrial dysfunction and morphology changes affect the maintenance and function of all major organs and tissues, such as the brain, heart, skeletal muscle, liver, and others the mechanisms contributing to early ovarian aging, a decrease of oocyte quality, and infertility remain unclear. In this review, we summarize the role of mitochondrial dysfunction in ovarian aging, presenting recent findings on morpho-functional changes in these organelles, and highlighting how their dysfunction accelerates ovary and cell senescence. We also explore their impact on oocyte functions. The reported data highlight the critical role of mitochondria in maintaining and enhancing oocyte quality, indicating that future studies should further focus on the mechanisms underlying mitochondrial damage and on identifying mitochondrial targets that may offer promising strategies to preserve, recover, and extend fertility in aging women.

Disruption of in mice resulted in male infertility with severe spermatogenesis defects. To investigate the molecular basis of infertility phenotype, we examined testicular proteomes of wild-type (WT) and mice using a mass spectrometry-based approach. We identified 727 and 525 differentially expressed proteins (DEPs) in 3- and 8-week old testes of mice, respectively, with an adjusted p-value cut-off of ≤ 0.05. Among these, 299 and 298 DEPs had fold change of ≥ 1.5 between WT and testes at -3- and 8-week old, respectively. In the 3-week old testes, 59.5% of the DEPs were up-regulated, while 40.5% were down-regulated. Similarly, in the 8-week old testes, 83.9% and 16.1% DEPs were up-regulated and down-regulated, respectively. Functional annotation and network analyses highlighted that many DEPs were associated with key biological processes, including ubiquitination, RNA processing, translation, protein folding, protein stabilization, metabolic processes, oxidation-reduction processes and sper-matogenesis. Subsequent immunohistochemistry and immunoblotting analyses showed higher ubiquitin levels in testes compared to WT, suggesting potential impairment in ubiquitin proteasome system (UPS) due to DCAF17 loss of function. Our data provide a basis for further work to elucidate the molecular function(s) of DCAF17 in spermatogenesis and male fertility.

Infertility and low birth rates have been threatening developed countries and have become a major socioeconomic problem that requires attention. To this end, germplasm preservation and subsequent fertility restoration with the aid of various assisted reproductive technologies (ART) have overcome many infertility issues over the last four decades. Particularly, cryopreservation offered various fertility preservation (FP) options for people with reproductive issues, gender dysphoria, and significantly expanded reproductive lifespan. The aim of this review is to provide the reader with the role that cryopreservation has played in human reproductive medicine (HRM) and family planning. We will first discuss the fundamentals of cryopreservation, including the development of cryopreservation methodologies for human reproductive cells and tissues, and how these techniques have helped address human infertility problems, as well as other ethical, legal, and social challenges. We will focus on literature regarding the current methodologies used in human infertility laboratories' clinical setting of the oocyte, sperm, and embryo, gonad cryopreservation, and discuss the latest issues related to the implementation of cryopreservation strategies used in HRM.