Jiaxin Zhang

This study aimed to systematically characterize the global research landscape, collaboration patterns, knowledge structure, and emerging hotspots of glucagon-like peptide-1 receptor agonists in neurodegenerative diseases using bibliometric methods. Publications related to glucagon-like peptide-1 receptor agonists and neurodegenerative diseases were retrieved from the Web of Science Core Collection from 2006 to 2025. Only English-language articles and reviews were included. Bibliometric analyses were performed using Bibliometrix, VOSviewer, and CiteSpace to evaluate annual publication trends, country and institutional contributions, author collaborations, journal distribution, citation structures, keyword co-occurrence, thematic evolution, and citation bursts. A Scopus-based sensitivity analysis was conducted to assess the robustness of the main bibliometric findings. A total of 1,202 publications were included, with annual output increasing from 2 in 2006 to 241 in 2025, particularly after 2020. China, the USA, and England were the leading contributors and major collaboration hubs. Shanxi Medical University, Lancaster University, and the National Institute on Aging were among the most productive institutions, while major journals included International Journal of Molecular Sciences, Neuropharmacology, European Journal of Pharmacology, Frontiers in Endocrinology, Frontiers in Pharmacology, and Journal of Alzheimer’s Disease. Keyword and citation analyses indicated a thematic shift from exendin-4, Alzheimer’s disease, Parkinson’s disease, and neuroprotection toward semaglutide, neuroinflammation, cognitive impairment, clinical efficacy, evidence synthesis, and combination therapy. Research on glucagon-like peptide-1 receptor agonists in neurodegenerative diseases has expanded rapidly over the past two decades. Current bibliometric evidence suggests that this field has evolved from preclinical exploration toward broader translational and clinical research, with increasing attention to neuroinflammation, metabolic dysfunction, cognitive outcomes, and newer incretin-based therapies. However, the therapeutic implications of glucagon-like peptide-1 receptor agonists for neurodegenerative diseases remain to be further validated by high-quality mechanistic studies and well-designed clinical trials.

Immune checkpoint inhibitors (ICIs) targeting PD-1/PD-L1 and CTLA-4 pathways have revolutionized cancer therapy, yet their efficacy is frequently limited by primary or secondary resistance. Emerging evidence underscores the gut microbiota as a decisive regulator of ICI therapeutic outcomes. This review systematically delineates the multi-dimensional mechanisms through which the microbiota modulates anti-tumor immunity, specifically focusing on the molecular remodeling of immune signaling by microbial metabolites such as short-chain fatty acids (SCFAs) and bile acids, cross-reactive immunity driven by antigenic molecular mimicry, and the spatial restructuring of the tumor microenvironment mediated by the gut-tumor axis. Clinically, fecal microbiota transplantation (FMT) has demonstrated the potential to reverse ICI resistance, while the development of live biotherapeutic products (LBPs) and precise prebiotic combinations offers a standardized path for niche-specific intervention. Despite these advances, critical challenges persist, including the biological mismatch in cross-species animal models, the context-dependency arising from individualized microbial signatures, and the cognitive gap in the temporal dynamics of microbe-drug interactions. Deciphering the non-linear correlation between microbial succession and host immune response will be essential for integrating microbiota-driven strategies into personalized oncology frameworks.

Obesity represents a significant global public health challenge, which not only elevates the risk of mortality but also increases the likelihood of chronic diseases. The ongoing obesity epidemic has led to a growing recognition of the detrimental effects of excessive adipose tissue accumulation on male reproductive health. Substantial evidence indicates that obesity adversely affects sperm quality, thereby impairing male fertility. Specifically, obesity is associated with compromised spermatogenesis, erectile dysfunction, and detrimental effects on offspring fertility parameters. These effects are mediated through various mechanisms, including alterations in the hypothalamic–pituitary–gonadal axis, inflammation within the reproductive system, localized caloric excess in reproductive tissues, epigenetic modifications, disruptions in gut microbiota, and heightened oxidative stress levels. While the molecular alterations associated with obesity have been extensively documented, the precise mechanisms by which obesity influences male reproductive function remain inadequately understood. This article aimed to review the classification and distribution of adipose tissue in obesity, the impact of obesity on male fertility, and the potential mechanisms through which obesity affects male reproductive health, thereby offering insights into the prevention and treatment of obesity-related male fertility issues.

Background: With the widespread use of static magnetic fields (SMFs) in applications such as magnetic resonance imaging (MRI) and electric vehicles, concerns have arisen regarding their potential effects on reproductive health. Despite increasing research, the impact of SMFs on reproductive function remains a subject of debate, requiring further exploration. Methods: This review synthesizes animal and clinical studies on the effects of SMF on reproductive function. It examines various SMF intensities and exposure durations, focusing on mitochondrial function, chromosomal division, and embryonic development. Results: The review reveals that low-intensity SMF exposure adversely affects mitochondrial function in sperm and eggs, reducing their activity. It also impacts follicular cells, delaying chromosomal division. Medium- and high-intensity SMF exposure shows mixed results, with both potential benefits and risks, requiring further research. High-intensity SMFs may pose teratogenic risks to embryos and delay the development of fertilized eggs. The position of SMF exposure also matters, likely due to field non-uniformity. Conclusions: This review provides a foundation for further investigation into the effects of SMFs on reproductive function, highlighting the need for more comprehensive studies to assess safety and applications. Special caution is advised for pregnant women regarding SMF exposure, given its potential risks.

Objective To investigate the associations of the gut microbiota with reproductive system diseases, including female infertility, male infertility, polycystic ovary syndrome (PCOS), primary ovarian failure, endometriosis, uterine fibroids, uterine polyps, sexual dysfunction, orchitis, and epididymitis. Methods A two-sample bidirectional Mendelian randomization (MR) analysis was performed to evaluate the potential causal relationship between the composition of gut microbiota and infertility, along with associated diseases. Results Sixteen strong causal associations between gut microbes and reproductive system diseases were identified. Sixty-one causal associations between gut microbes and reproductive system diseases were determined. The genus Eubacterium hallii was a protective factor against premature ovarian failure and a pathogenic factor of endometriosis. The genus Erysipelatoclostridium was the pathogenic factor of many diseases, such as PCOS, endometriosis, epididymitis, and orchitis. The genus Intestinibacter is a pathogenic factor of male infertility and sexual dysfunction. The family Clostridiaceae 1 was a protective factor against uterine polyps and a pathogenic factor of orchitis and epididymitis. The results of reverse causal association analysis revealed that endometriosis, orchitis, and epididymitis all led to a decrease in the abundance of bifidobacteria and that female infertility-related diseases had a greater impact on gut microbes than male infertility-related diseases did. Conclusions The findings from the MR analysis indicate that there is a bidirectional causal relationship between the gut microbiota and infertility as well as associated ailments. Compared with ovarian diseases, uterine diseases are more likely to lead to changes in women’s gut microbiota. The findings of this research offer valuable perspectives on the mechanism and clinical investigation of reproductive system diseases caused by microorganisms.

The male reproductive immune system plays a pivotal role in safeguarding sperm from immune attacks and preventing the incursion of foreign pathogens. Nucleotide-binding and oligomerization domain-like receptors (NOD-like receptors, NLRs) family protein domain containing 3 (NLRP3) is a cytoplasmic sensor binding to the inflammasome and critically involved in inducing innate immunity in the testes. It also has a substantial impact on male reproductive immunity, which is closely associated with male infertility stemming from disorders related to the male reproductive immune system. This review introduces the distinct characteristics of the NLR family, elucidates the activation pathways and factors of NLRP3 inflammasomes, and discusses how they participate in male reproductive immune diseases such as bacterial orchitis, autoimmune orchitis, varicocele, and epididymitis. In bacterial orchitis, elevated levels of NLRP3 inflammasomes exacerbate the testicular inflammatory injury and lead to decreased testosterone, thus contributing to male infertility. In autoimmune orchitis, the NLRP3 inflammasomes inhibit testosterone synthesis by decreasing the expression of cytochrome P450, thereby impacting male reproductive function. Therefore, targeting NLRP3 could offer novel immunological strategies for the clinical treatment of male infertility.