China ranks first in the number of publications in this field, followed by the United States. The publication output of these two countries far exceeds that of others, indicating the significant interest of researchers in both countries and their substantial investment in research related to gut microbiota and HUA. Among the top 10 institutions in terms of publications, the top institution in terms of both publications and citations is UCSD in the United States, and the remaining 9 institutions are from China. UCSD has close collaboration with leading institutions such as Qingdao University and the Chinese Academy of Sciences. Professor Changgui Li from the Department of Endocrinology and Metabolism at the Affiliated Hospital of Qingdao University, Professor Huiyong Yin from the Chinese Academy of Sciences, and expert Robert Terkeltaub from UCSD worked together to discover differentially abundant metabolites and pathways underlying infrequent gout flares (InGFs) and frequent gout flares (FrGFs) through metabolomics and to establish a predictive model via machine learning (ML) algorithms (Wang M. et al., 2023). Notably, Robert Terkeltaub contributed to the American College of Rheumatology’s gout management guidelines (Khanna et al., 2012). Additionally, Professor Changgui Li serves as co-chair of the Asia–Pacific Gout Consortium (APGC)² and plays a leading role in the field of gout and HUA, potentially laying the groundwork for collaboration among various organizations.

Analysis of authors and co-cited authors demonstrates that Sanjay K. Nigam is an influential writer who has made significant contributions to the fields of HUA and the intestinal microbiota. A 2015 review by Sanjay K. Nigam, published in Physiological Reviews, stands out as a representative work. This review underscores the essential functions of organic anion transporter 1 (OAT1) and OAT3 in the metabolism and processing of gut microbiome metabolites (Nigam et al., 2015). These transporters are predominantly expressed in the proximal tubule cells of the kidney, where they facilitate the transport of organic anions, such as UA, from the bloodstream into cells, subsequently expelling them through the cell’s apical membrane into the urine. OAT1 and OAT3 are particularly critical in the transmembrane transport of UA, a process they facilitate by exchanging dihydroxyacetate within the cell (Otani et al., 2017). In 2019, Sanjay K. Nigam’s team constructed a co-expression network of the gut-liver-kidney (GLK) axis, revealing interactions between transport proteins (e.g., OAT1, OAT3, and URAT1) and metabolizing enzymes (e.g., CYP4A11 and UGT2B4) associated with UA metabolism, emphasizing the role of these genes in regulating UA levels and intestinal flora metabolite transport (Rosenthal et al., 2019). In 2020 and 2022, it was noted that OAT1 and OAT3 are involved in UA reabsorption and excretion in renal proximal tubules and interact with gut flora metabolites (e.g., indoleacetic acid and 4-hydroxyphenylacetic acid) to affect UA levels, which in turn affects the progression of CKD (Engelhart et al., 2020; Granados et al., 2022; Jamshidi and Nigam, 2022). In 2023, it was found that gut microbiota metabolites, including tryptophan derivatives, could activate the host’s OATs and aryl hydrocarbon receptor (AHR), impacting UA secretion and excretion, thus creating a remote sensing and signaling mechanism between UA metabolism and intestinal flora, which is particularly important in chronic kidney disease (Nigam and Granados, 2023). In addition, loss of function of transporter proteins such as OAT1 leads to changes in the composition and function of the intestinal flora, thereby affecting UA metabolism (Ermakov et al., 2023). The research of Professors Sanjay K. Nigam et al. revealed the core bridging role of OAT1/OAT3 in the interaction between UA metabolism and intestinal microbiota, constructed the theoretical framework of the GLK axis, and laid a revolutionary theoretical foundation for the mechanism research, prevention, and treatment of hyperuricemia and chronic kidney disease.

A total of 736 documents appeared in 369 different journals, with major contributions from respected sources like Nutrients, Frontiers in Microbiology, and Food & Function. Interestingly, the Nutrients stood out as a primary focus, with a significant number of published studies and citations. This recognition confirms the Nutrients’ position as a significant outlet for sharing research findings in the field of gut microbiota and HUA and highlights the publication’s importance in this sector.

References with the strongest citation bursts analysis reveal the most influential references in the field. The citation boom period in this field is relatively concentrated, mainly occurring between 2017 and 2022. The citation research content that emerged at this stage was quite rich, including the description of the microbiota of clinical patients and microecological intervention strategies (including probiotics for lowering UA, dietary fiber for promoting the generation of SCFAs, tuna oligopeptides for repairing the intestinal barrier, etc.) (Guo et al., 2016; Shao et al., 2017; García-Arroyo et al., 2018; Han et al., 2020). Published in 2016 in Scientific Reports, the paper “Intestinal Microbiota Distinguish Gout Patients from Healthy Humans” experienced the strongest citation burst (strength = 17.67) between 2017 and 2021. This is a clinical cohort study, which revealed significant differences in the intestinal microflora between gout patients and healthy individuals. Bacteroides xylanisolvens and Bacteroides caccae were more abundant in gout patients, whereas Bifidobacterium pseudocatenulatum and Faecalibacterium prausnitzii were less abundant (Guo et al., 2016). The second strongest citation burst (strength = 13.27) article, titled “Combined Signature of the Fecal Microbiome and Metabolome in Patients with Gout,” was published by Shao et al. (2017) in the journal Frontiers in Microbiology. This study examined the fecal microbiome signatures and revealed an increase in pathogens, including Erysipelatoclostridium, Rhodococcus, Anaerolineaceae, and Bacteroides. The metabolome signatures included altered metabolites that may play a role in inflammatory responses, purine metabolism, and UA excretion (Shao et al., 2017). The third most intense citation burst (strength = 8.8) is an article titled “Alterations of the Gut Microbiome Associated With the Treatment of Hyperuricaemia in Male Rats,” published by Yu et al. (2018) in the journal Frontiers in Microbiology. The study investigates the effects of allopurinol and benzbromarone on the gut microbiota of male rats with hyperuricaemia, revealing specific alterations in bacterial genera and metabolic pathways associated with nucleotide and lipid metabolism (Yu et al., 2018). In addition, several papers that are still in the explosive period (2022–2024) indicate that the functional differences of gout subtypes in the microbiota and the deepening of probiotic mechanisms in this field have been studied (Méndez-Salazar et al., 2021; Ni et al., 2021).

Through keyword co-occurrence and timeline visualization graphs, a large number of microbiota names, such as “gut microbiota,” “Bifidobacteria,” and “Escherichia coli,” were discovered, indicating that various types of microbiota have always been the focus of attention in this field. Multiple studies have shown that compared with healthy individuals, there are significant differences in the diversity and composition of the gut microbiota in patients with HUA (Table 5 and Supplementary Table 1). These differences are not only reflected in the “rise and fall” of specific bacterial genera, but also reflect the dual impact of the imbalance in the interaction between the microbiota and the host on metabolism and inflammation. Firstly, the enrichment of SCFAs-producing genera such as Alistipes, Faecalibacterium, and Roseburia has been repeatedly reported (Lin et al., 2021; Yuan et al., 2022). These bacteria may constitute a compensatory mechanism by which the body attempts to alleviate hyperuric acid-related metabolic disorders by maintaining the integrity of the intestinal barrier and inhibiting inflammatory responses. Secondly, multiple studies have reported that serum UA levels are positively correlated with the abundance of Bacteroides in patients with HUA/gout (Guo et al., 2016; Shao et al., 2017; Méndez-Salazar et al., 2021). Although research reports have found that Bacteroides are one of the main enterotypes in the healthy population of South Korea, and 5-hydroxyisourate hydrolase, involved in the conversion of UA to allantoin, is enriched in this type of intestinal type (Lim et al., 2014). However, most studies have found that Bacteroides are involved in pro-inflammatory effects under disease conditions. For instance, B. caccae have been identified as biomarkers of inflammatory bowel disease (IBD) (Wei et al., 2001). Additionally, an increased presence of Bacteroides spp. has been linked to various autoimmune diseases, including systemic lupus erythematosus (Hevia et al., 2014), rheumatoid arthritis (Zhang et al., 2015), and type 1 diabetes (Davis-Richardson and Triplett, 2015). It is suggested that the amplification of Bacteroides may simultaneously trigger chronic inflammation. Third, the general reduction of probiotics such as Bifidobacteria (Guo et al., 2016; Lin et al., 2021; Méndez-Salazar et al., 2021; Yang et al., 2021; Ul-Haq et al., 2022). Bifidobacteria are renowned for their probiotic properties and anti-inflammatory effects, and their depletion may contribute to the overall dysbiosis and elevated inflammatory levels in HUA patients (Ruiz et al., 2017). In addition, the imbalance of opportunistic pathogenic bacteria (such as Porphyromonas and Enterobacteriaceae) and SCFA-producing beneficial bacteria (such as Clostridium and Ruminococcus) further amplifies the risk of inflammation. It is worth noting that the abundance changes of Prevotella show contradictory results in different studies (Ul-Haq et al., 2022; Martínez-Nava et al., 2023). This discrepancy highlights the influence of confounding factors such as disease stage, diet, and testing methods on the dynamics of the microbiota (Wu et al., 2011). In conclusion, the intestinal microbiota of patients with HUA shows a pattern of “pro-inflammatory-anti-inflammatory” bacterial growth and decline. This imbalance pattern may either be the result of metabolic disorders or exacerbate hyperuricemia and inflammation through gut-axis feedback. In the future, it is necessary to combine longitudinal cohorts and standardized analyses to clarify the causal roles and individual heterogeneity of the changes in the microbiota. Meanwhile, the specific mechanism of action of Bacteroides under different physiological and pathological conditions should be further explored to provide more comprehensive theoretical support for the prevention and treatment of hyperuricemia and related diseases.

Through high-frequency keywords, keyword clustering, and citation burst analysis, we found that “probiotics,” “prebiotics,” and “therapy” are important research topics in the field of gut microbiota in hyperuricemia. The mechanism of probiotics in treating HUA includes altering the composition of the intestinal microbiota. Probiotics regulate the composition of the gut microbiota by increasing the abundance of beneficial bacteria (such as Bifidobacteria, Prevotella, Firmicutes, and SCFA-producing bacteria) while reducing pathogenic or pro-inflammatory bacteria (such as Bacteroidetes and Enterococcus). For instance, researchers have shown that Lactobacillus plantarum LLY-606 and L. plantarum TCI227 enhance the production of SCFAs and decrease the abundance of harmful bacteria such as Escherichia/Shigella (Chien et al., 2022; Shi et al., 2023). This modulation of the gut microbiota is considered a key mechanism underlying the therapeutic efficacy of probiotics. Secondly, it inhibits the activity of XOD. XOD is a pivotal enzyme in the biosynthesis of UA. Several probiotic strains (including Lactobacillus rhamnosus Fmb14, L. plantarum Q7, and Lactobacillus DM9218) have been shown to inhibit XOD activity in the liver, subsequently reducing UA concentrations (Wang et al., 2019; Ni et al., 2021; Cao et al., 2022; Li et al., 2022; Zhao et al., 2022; Shi et al., 2023). Additionally, probiotics can modulate the expression of UA transporter proteins, such as ABCG2, GLUT9, and URAT1 (Zhao et al., 2022; Wang Z. et al., 2023). These observations underscore the potential of probiotics to exert a direct influence on UA metabolism. Furthermore, numerous probiotics demonstrate notable anti-inflammatory properties by diminishing the expression of pro-inflammatory cytokines, including IL-1β, TNF-α, and IL-6. For instance, L. rhamnosus Fmb14 and L. plantarum LLY-606 have been shown to downregulate IL-1β and TNF-α levels, thereby mitigating inflammation associated with HUA (Li et al., 2022; Shi et al., 2023). Supplementary Table 2 details the specific mechanisms.

In addition, keyword co-occurrence reveals that the high-frequency keywords “growth performance,” “broiler chickens,” and “probiotics” are linked to each other. It is indicated that adding probiotics to regulate the UA level in broilers and improve their growth performance and meat quality is also a research hotspot on this topic. For instance, studies have shown that Lactobacillus farciminis CNMA67-4R, Clostridium butyricum CBM 588, multi-strain probiotics, and symbiotics (Bacillus subtilis, inulin, and Saccharomyces cerevisiae) significantly reduced the UA levels in the feces of broiler chickens, which is the primary substrate for ammonia production. Moreover, L. farciminis CNMA67-4R and the symbiotics decreased the urine nitrogen ratio in the feces, thereby leading to a reduction in ammonia emissions from the chickens (Such et al., 2021; Such et al., 2023). The reduction of ammonia emissions is of considerable importance for environmental protection and animal welfare, and it can also enhance the growth performance and immune function of broiler chickens. The timeline visualization map shows that “fecal microbiota transplantation,” “fermentation,” and “extract” are the key research topics in recent years. It indicates that, in addition to probiotics, other microbiota-based treatments [such as microbiota transplantation and microbial fermentation extracts (MFEs)] have received extensive attention. Liu et al. (2020) found that FMT effectively modulated the gut microbiota in rats with high-purine-induced HUA, leading to improvements in metabolic parameters. Furthermore, in patients with gout, washing microbiota transplantation decreases serum UA levels, is related to a reduction in both the frequency and duration of acute gout flares, lowers diamine oxidase and endotoxin levels, and helps improve their impaired intestinal barrier function (Xie et al., 2022). Treatment with Lactobacillus acidophilus fermented dandelion (LAFD) has been shown to restore imbalances in the gut microbial ecosystem and reverse alterations in Bacteroidetes/Firmicutes, Muribaculaceae, and Lachnospiraceae in HUA mice (Ma et al., 2023). In addition, research indicates that certain MFEs did not exhibit systemic toxicity even at high doses, suggesting a favorable safety and efficacy profile for the treatment and prevention of HUA (Chen et al., 2017). In conclusion, the technique of bacterial colony transplantation and its associated microbial fermentation products hold promise for the treatment of HUA.

However, in practical applications, probiotics face multiple challenges in the management of HUA. Firstly, ensuring a high viable bacterial count and stability of probiotics during processing, storage, transportation, and after passing through harsh gastrointestinal environments such as gastric acid and bile is crucial. Although encapsulation technology can enhance targeted delivery and viability, its effectiveness and repeatability still need to be optimized (Broeckx et al., 2016; Cassani et al., 2020; Sun et al., 2023). Secondly, significant individual differences in therapeutic effects exist, influenced by the composition of the host’s intestinal flora, genetic background, and lifestyle factors such as diet and medication (Sun et al., 2024; Wang Q. et al., 2024). This highlights the necessity of personalized strain and dosage selection. Finally, the current regulatory and standardization framework is still not perfect. There is a lack of unified standards for strain identification, evaluation, and quality control. It is urgent to implement stricter quality control procedures (such as ensuring the consistency between the actual content of the product and the label statement and preventing contamination) and adopt genomic assessment methods to verify the safety and accuracy of strains, to enhance product quality, safety, and consumer trust (Salvetti et al., 2016; Kolaček et al., 2017).

Keyword co-occurrence and timeline visualization analysis reveal that “polysaccharides,” “diet,” and “dietary fiber” are important research topics in this field, indicating that both traditional Chinese medicine (TCM) and dietary patterns regard the intestinal flora as the hub target for regulating HUA. They exert their effects through a two-way intervention strategy: on the one hand, they inhibit “dangerous bacteria” such as Bacteroidetes and Enterobacteriaceae that produce endotoxins and promote inflammation; on the other hand, they increase beneficial bacterial species such as Lactobacillus, Bifidobacterium, and Roseburia that produce SCFAs and strengthen the gut-kidney axis. Ultimately, they jointly reduce the UA load, decrease oxidative stress and inflammation, and achieve multi-layered benefits from the structure of the microbiota to the host’s metabolic-immune-kidney function.

The active ingredients of TCM and the intestinal flora synergistically intervene in UA homeostasis through a “bidirectional metabolism-regulation” model. Some bioactive ingredients in TCM are not effectively absorbed in the digestive tract, causing low bioavailability (Gong et al., 2020). On the one hand, TCM is first enzymatically hydrolyzed by the microbiota to generate more easily absorbed active metabolites, such as baicalin being converted into baicalein before entering the bloodstream (Noh et al., 2016), and the host metabolism is indirectly regulated through SCFAs and other microbiota products (Wang et al., 2017); on the other hand, active ingredients reshape the structure of the microbiota. Tea polyphenols, berberine, etc., can inhibit harmful bacteria, promote the growth of beneficial bacteria, improve microecology, and UA metabolism (Yan et al., 2020; Chen Q. et al., 2023; Wang L. et al., 2023). This bidirectional network provides new ideas for explaining the mechanism of action of TCM and developing microbiogenic therapies. However, most of the existing evidence remains at the animal model level, and the causal chain has not yet been fully verified in the human body. Among polyphenols, resveratrol (from Polygonum cuspidatum) was shown to increase Lactobacillus spp. and SCFA-producing bacteria (e.g., Clostridium and Bifidobacterium), while reducing Bacteroides and pro-inflammatory cytokines (IL-6, IL-1β, and TNF-α) (Zhou Y. et al., 2024). Chlorogenic acid (from Lonicera japonica) was observed to inhibit TMAO-synthesizing bacteria (Faecalibaculum and Blautia) and activate the PI3K/AKT/mTOR pathway, reducing renal fibrosis and oxidative stress (Zhou et al., 2022). Furthermore, ferulic acid (from Ligusticum chuanxiong) remodeled gut microbiota in HUA rats, while inhibiting the TLR4/NF-κB pathway to reduce UA absorption (Zhang N. et al., 2023). Among flavonoids, quercetin (from Taxillus chinensis) reduced hepatic XOD activity and enhanced purine degradation in HUA mice, with Lactobacillus aviarius implicated in UA metabolism modulation (Li D. et al., 2023). Myricetin-Nobiletin Hybrid (from waxberry and Citrus reticulata) regulated glycerophospholipid metabolism and increased norank_f_Muribaculaceae abundance in HUA mice, ameliorating renal damage (Li Y. et al., 2023). Saffron flavonoid extract (from Crocus sativus) reversed HUA-induced dysbiosis by enriching beneficial genera (Roseburia and Clostridium sp.) and suppressing pathogens (Alloprevotella and Parabacteroides) in rats, while enhancing antioxidant activity (Chen et al., 2022). Regarding alkaloids, berberine (from Coptis chinensis) upregulated colonic ABCG2 and reduced Bacteroidetes in HUA rats, enriching Lactobacillus and promoting UA excretion (Chen Q. et al., 2023). The classification of active ingredients in TCM, as well as their mechanisms of action and targeted bacterial communities, is shown in Supplementary Table 3.

In addition, diuretic and turbidium-reducing herbs have also demonstrated consistent effects in animal models, such as enhancing probiotics, reducing pathogenic bacteria, and lowering UA. Kidney tea has been observed to significantly enhance the abundance of Roseburia and Enterorhabdus, while reducing the abundance of Ileibacterium and UBA1819 in HUA model mice (Chen Y. et al., 2023). In addition, Chicory promotes probiotic growth and pathogen reduction to aid UA excretion in HUA quail (Bian et al., 2020). Additionally, Camellia sinensis increases the abundance of Ruminococcus and Lactobacillus, decreases the abundance of Bacteroides and E. coli, and regulates UA metabolism in HUA mice (Wu et al., 2022). Although preclinical studies based on rodent models suggest that TCM and its components may intervene in HUA by regulating the intestinal flora and UA metabolism, there is still significant uncertainty regarding its clinical transformation. The key limitation lies in the lack of high-quality clinical trials to verify the mechanism of action mediated by microorganisms. It is difficult to establish a causal relationship in multi-component compound prescriptions where specific components drive microbial changes and mechanically reduce UA. The methodological heterogeneity existing in preclinical studies (such as differences in HUA induction regimens, administration doses/dosage forms, and microbiota analysis techniques) restricts the direct comparability and universality of the results. Furthermore, the long-term sustainability impact of significant baseline microbiota differences among individuals on intervention responses and induced changes urgently needs in-depth exploration. Future research should enhance high-quality clinical trials, adopt uniform standards, systematically evaluate the impact of TCM on HUA, and take into account individual differences in microbiota to formulate personalized treatment plans. Figure 9 demonstrates the mechanisms by which probiotics and TCM mitigate HUA through modulation of the gut microbiota.

Different dietary patterns significantly influence the composition and function of gut microbiota, which in turn affects the management of HUA. A study has demonstrated that dietary patterns characterized by high intake of animal protein, fat, and alcohol are positively correlated with the prevalence of HUA, whereas diets abundant in fruits, vegetables, legumes, and grains are inversely associated with HUA prevalence (Teng et al., 2015). The key components of these dietary patterns regulate UA levels through specific interactions with gut microbiota and their metabolic outputs. For example, Western dietary patterns, characterized by elevated intake of saturated fats and animal proteins, induce dysbiosis of the intestinal flora (Huang et al., 2013). The microbiota characteristics of animal models induced by long-term high-fat and high-fructose diets also support this view (Zhang N. et al., 2023). This dysbiosis increases intestinal permeability and stimulates the release of pro-inflammatory mediators (e.g., LPS, TNF-α, and IL-1β) and diminishes the production of SCFAs, particularly butyrate, which has anti-inflammatory properties and may enhance renal UA excretion (Chu et al., 2021; Li et al., 2021; Xu et al., 2021). In addition, researchers have found that SCFAs enhance the excretion of intestinal UA by activating peroxisome proliferator-activated receptor γ (PPARγ), which binds to the ABCG2 promoter (Adeyanju et al., 2021; Li M. et al., 2023). Conversely, the Mediterranean dietary (e.g., fruits, vegetables, nuts, whole grains, and beans) pattern, abundant in vitamins, minerals, polyphenols, dietary fiber, and monounsaturated fatty acids (MUFAs), fosters the proliferation of Bifidobacteria and Lactobacillus, and improve gut health by increasing the production of SCFAs while mitigating cells inflammatory responses lowering concentrations of TMAO, thus exerting a favorable effect on UA reduction (Chrysohoou et al., 2011; Chatzipavlou et al., 2014; Cariello et al., 2020; Soldán et al., 2024). Research has demonstrated that in hyperuricemia nephropathy rats, there was a significant increase in Blautia, Enterococcus, and Faecalibaculum associated with TMAO production. TMAO activates PI3K/AKT/mTOR signaling pathway, induces local inflammatory reaction in the kidney, aggravates kidney fibrosis, destabilizes UA transport proteins, and diminishes the kidney’s UA excretion capacity (Zhou et al., 2022). In addition, The Dietary Approaches to Stop Hypertension (DASH) diet, which emphasizes plant-based foods rich in whole grains, fruits, vegetables, and low-fat dairy products, has been shown to significantly enhance the abundance of beneficial gut microbiota such as Bifidobacterium and Lactobacillus, while reducing the prevalence of harmful bacteria, including LPS-producing Enterobacteriaceae. These beneficial microbial populations contribute to the reduction of UA levels through the production of SCFAs and the inhibition of XOD activity (Martínez et al., 2010; Gong et al., 2018; Ashaolu, 2020; Aslam et al., 2020). These findings underscore the significant role of dietary patterns in managing HUA by modulating the composition and function of the gut microbiome. Furthermore, selecting diets rich in dietary fiber and polyphenols may aid in lowering UA levels and alleviating symptoms in individuals with HUA.

Timeline visualization analysis revealed that “liver,” “kidney,” “gut-kidney axis,” etc. have also been research hotspots in recent years. It has attracted much attention in recent years that the gut microbiota, through a multi-dimensional network composed of four axes including gut-kidney, gut-liver, gut-joint, and gut-brain, collaboratively regulates UA homeostasis in distant organs. On the gut-kidney axis, probiotics (such as L. rhamnosus) directly upregulate colonic UA transporters (such as ABCG2), accelerating UA excretion to reduce blood UA (Wang H. et al., 2024). Its metabolites, SCFAs, indirectly maintain UA balance by strengthening the intestinal barrier and inhibiting the TLR4/NLRP3 inflammatory pathway (Bi et al., 2024; Wang Q. et al., 2024; Lv et al., 2025). In the gut-liver axis, specific strains (Lactobacillus reuteri and Lactobacillus johnsonii) also promote UA excretion by enhancing barrier function and transporter protein expression, while further reducing blood UA by utilizing purine metabolism and using UA as a carbon source (Kasahara et al., 2023; Hussain et al., 2024; Han et al., 2025). The combination of probiotics with ursolic acid and oleanolic acid can reshape the structure of the microbiota, synergistically inhibit liver inflammatory pathways, and optimize UA metabolism (Ma et al., 2020). On the gut-joint axis, the barrier disruption mediated by TLR4/NLRP3 inflammation hinders UA excretion, while 7-ketocholic acid promotes epithelial repair by inhibiting FXR (Li et al., 2024; Wang Q. et al., 2024). Probiotics enrich Lactobacillus and Faecalibacterium through tryptophan metabolism, enhance the UA transport function of the colon, and indirectly reduce the risk of hyperuricemia. The gut-brain axis enhances the barrier through strains such as L. reuteri, upregulates the production of ABCG2 and SCFAs, transmits signals to the central nervous system via the vagus nerve, and regulates the synthesis and excretion of UA (Cryan et al., 2019; Wang et al., 2020; Hussain et al., 2024). In conclusion, the collaborative network of microbiota, metabolites, transport proteins, and distal organs provides a new microbiogenic intervention strategy for hyperuricemia.