International journal of molecular medicine最新文献

{"title":"RBM8A promotes gastric cancer progression by binding with UPF3B to induce BBC3 mRNA degradation.","authors":"Hang Peng, Long Zhang, Fang Li, Xintao Jing, Jing Zhou, Li Cao, Cuixiang Xu, Jianhua Wang, Chen Huang","doi":"10.3892/ijmm.2025.5572","DOIUrl":"10.3892/ijmm.2025.5572","url":null,"abstract":"<p><p> RNA metabolism is an important post‑transcriptional regulatory mode in organisms, and its process is cooperatively regulated by a variety of RNA‑binding proteins. RNA binding motif protein 8A (RBM8A), a regulator of mRNA stability that is implicated in cancer progression, serves an important role in processes such as RNA splicing, transport, translation and decay. However, to the best of our knowledge, its role in the occurrence and development of gastric cancer (GC), as well as its biological functions and molecular mechanisms remain unclear. In the present study, RBM8A expression was on average 1.4‑fold higher (P<0.05), with a maximum log2 fold change of 1.4 (2.6‑fold increase), in GC tissues compared with adjacent normal tissues, as determined by multiplex immunohistochemical analysis of tissue microarrays. <i>In vitro</i>, transfection of RBM8A small interfering RNAs significantly suppressed the proliferation of AGS and HGC27 cells and enhanced apoptosis. Specifically, annexin V‑positive AGS cells exhibited a 2.9‑fold increase with siRBM8A‑1 transfection and a 1.9‑fold increase with siRBM8A‑2 transfection, while annexin V‑positive HGC27 cells exhibited a 2.3‑fold increase with siRBM8A‑1 transfection and a 1.8‑fold increase with siRBM8A‑2 transfection (P<0.05). Using MKN45 cell lines and subcutaneous xenograft models, the present study revealed that RBM8A knockdown reduced subcutaneous tumor growth in nude mice by 51.5% in terms of volume and 62.4% in terms of weight (P<0.05). In terms of the mechanism, integrated mRNA‑sequencing (seq) and RNA immunoprecipitation (RIP)‑seq identified BCL2 binding component 3 (BBC3), a well‑characterized pro‑apoptotic gene, as a direct target of RBM8A. Further results of RIP‑quantitative PCR, fluorescence <i>in situ</i> hybridization‑immunofluorescence and RNA pulldown indicated the direct interaction between RBM8A and BBC3 mRNA. Actinomycin D assays demonstrated that RBM8A promoted BBC3 mRNA degradation. Subsequently, the co‑immunoprecipitation assay showed that RBM8A interacted with UPF3B to jointly regulate the stability of BBC3 mRNA. In conclusion, RBM8A inhibited apoptosis and promoted GC progression by interacting with UPF3B, leading to degradation of the pro‑apoptotic gene BBC3 mRNA. These findings highlighted that interfering with RBM8A expression, or disrupting the interactions between RBM8A and BBC3 mRNA or between RBM8A and UPF3B could serve as potential therapeutic strategies for GC.</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"56 3","pages":""},"PeriodicalIF":5.7,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12236746/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144560128","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effects of anti‑VEGF on peripapillary retinal nerve fiber layer and papillary/peripapillary blood circulation in retinopathies (Review).","authors":"Hongwei Wang, Renfeng Ding, Wenya Jiang, Siyi Li, Yijuan Wu, Junfeng Mao, Yanan Chen, Peng Sun, Mengqi Shi","doi":"10.3892/ijmm.2025.5574","DOIUrl":"https://doi.org/10.3892/ijmm.2025.5574","url":null,"abstract":"<p><p>Vascular endothelial growth factor (VEGF) is an endothelial cell‑specific angiogenic factor. VEGF is involved in vasodilatation, nerve protection and retinal development and maturation. Over‑expression of VEGF is closely associated with retinopathies, such as retinal vein occlusion, diabetic retinopathy, age‑related macular degeneration and diabetic macular edema. Intravitreal injections of anti‑VEGFs are widely used in the treatment of retinopathies to reduce the angiogenesis and the macular edema. Hypothetically, repeated anti‑VEGF injections for retinopathies should interfere with the neuroprotective function of VEGF and might induce the vasoconstriction with a subsequent decrease in the ocular perfusion. These two could affect the optic nerve. The peripapillary retinal nerve fiber layer (p‑RNFL) thinning and the decreased papillary/peripapillary blood circulation can show the optic nerve damage earlier. In the present review, the effects of anti‑VEGFs on p‑RNFL and papillary/peripapillary blood circulation in retinopathies were comprehensively summarized and analyzed to explore whether the anti‑VEGFs cause damages to the optic nerve. The present review provided a detailed evaluation and analysis of the changes in p‑RNFL thickness, papillary/peripapillary blood circulation and intraocular pressure and the correlations between these changes with the number and type of anti‑VEGFs in 3,078 affected eyes and 520 fellow eyes with retinopathies. The present review sought to establish a foundation for the intravitreal administration of anti‑VEGFs and efficacy monitoring of the possible side effects on the optic nerve.</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"56 3","pages":""},"PeriodicalIF":5.7,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144560125","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Blood‑brain barrier dysfunction in epilepsy: Mechanisms, therapeutic strategies and future orientation (Review).","authors":"Na Huang, Yawen Huang, Zhenyuan Deng, Shuya Qi, Wei Zhang, Yuanyuan Liu, Guohe Tan","doi":"10.3892/ijmm.2025.5577","DOIUrl":"10.3892/ijmm.2025.5577","url":null,"abstract":"<p><p>The blood‑brain barrier (BBB) is a crucial structure for maintaining homeostasis within the central nervous system, and its integrity plays a pivotal role in the onset and progression of epilepsy. Epileptic seizures can disrupt the molecular architecture of the BBB, including the loss of tight junction proteins, activation of matrix metalloproteinases and dysfunction of supporting cells. Various pathological changes, such as transmembrane transport disorders, upregulation of platelet‑derived growth factor receptor β and vascular endothelial growth factor signalling pathways, and activation of astrocytes and microglia, accompany these alterations. These modifications exacerbate the entry of toxic molecules (such as albumin) into the brain parenchyma, triggering neuroinflammation and neuronal damage, thereby establishing a vicious cycle of epilepsy, BBB disruption and recurrent epilepsy. Consequently, repairing or protecting the BBB is a novel strategy for controlling epileptic seizures and treating drug‑resistant epilepsy. Consequently, compared with current treatment approaches that primarily focus on suppressing neuronal excitability, repairing or protecting the BBB is a novel strategy for controlling epileptic seizures and treating drug‑resistant epilepsy. Drugs such as botulinum, levetiracetam and angiotensin receptor blockers show the potential for BBB protection. The development of nanomaterials can enhance drug concentrations in affected areas, thereby offering new avenues for refractory epilepsy. The present study systematically reviews the critical role of the BBB in the pathogenesis of epilepsy, untangles the complex association between BBB dysfunction and the course of the disease, aims to deepen our understanding of the molecular mechanisms underlying BBB damage, and explores new approaches for epilepsy prevention and treatment from a BBB perspective. This review provides a theoretical foundation and research direction for the development of diagnostic and treatment strategies that are safer and more effective than current standard therapies.</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"56 3","pages":""},"PeriodicalIF":5.7,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144560124","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Histone deacetylase 6: A new player in oxidative stress‑associated disorders and cancers (Review).","authors":"Fei Qu, Qingqing Zhao, Yi Jin","doi":"10.3892/ijmm.2025.5578","DOIUrl":"https://doi.org/10.3892/ijmm.2025.5578","url":null,"abstract":"<p><p>Histone deacetylase 6 (HDAC6), a distinctive member of the histone deacetylase family, plays a crucial role in regulating the cellular response to oxidative stress. Unlike other HDACs, HDAC6 primarily deacetylates non‑histone proteins, influencing various cellular functions critical to the pathogenesis of numerous oxidative stress‑related diseases. This review summarizes the latest research on how HDAC6 affects oxidative stress pathways and its impact on diseases such as neurodegeneration, cancer and cardiovascular disorders. Additionally, the therapeutic potential of targeting HDAC6, as evidenced by preclinical trials, was discussed, suggesting that HDAC6 inhibitors can ameliorate symptoms and alter disease progression in numerous disease models. By elucidating the multifaceted roles of HDAC6 in oxidative stress and disease, the review aims to underscore its potential as a therapeutic target. This review enhances the understanding of HDAC6 and presents new opportunities for innovative treatment approaches that can address oxidative stress‑related illnesses.</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"56 3","pages":""},"PeriodicalIF":5.7,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144608307","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Benzo[a]pyrene aggravated ovalbumin‑induced epithelial tight junction disruption via ROS driven‑NLRP3/Caspase‑1 signaling pathway in asthmatic mice.","authors":"Yanqiu Xu, Yanming Feng, Ling Wang, Xin Xu, Li Xu, Bohan Wang","doi":"10.3892/ijmm.2025.5573","DOIUrl":"10.3892/ijmm.2025.5573","url":null,"abstract":"<p><p>Air pollutants contribute to the occurrence and development of asthma by impairing the airway epithelial barrier. However, underlying molecular mechanisms remain unknown. The present study investigated whether co‑exposure to the air pollutant benzo[a]pyrene (BaP) and ovalbumin (OVA) enhanced OVA‑induced epithelial tight junction disruption and explored the potential mechanisms involved. Asthma mouse and airway epithelial cell models were established and exposed to BaP. Lung pathology, immunoglobulin E (IgE), tight junction proteins zonula occludens‑1 (ZO‑1) and occludin, reactive oxygen species (ROS), NOD‑like receptor protein 3 (NLRP3), apoptosis‑associated speck‑like protein containing a CARD, caspase‑1, interleukin (IL)‑18 and IL‑1β were assessed by hematoxylin‑eosin staining, enzyme‑linked immunosorbent assay, western blotting, immunohistochemistry and immunofluorescence. Inhibitors of ROS and NLRP3 were used to assess their effect on ZO‑1 and occludin and downstream signaling pathways to clarify BaP‑induced damage. Lung tissue damage was exacerbated by BaP, the IgE level increased and the ZO‑1 and occludin expression reduced in both models, thereby disrupting airway epithelial tight junctions. Additionally, BaP increased ROS levels and activated the NLRP3/caspase‑1 signaling pathway. However, reducing ROS and NLRP3 restored the ZO‑1 and occludin expression and improved epithelial integrity. Airway tight junction disruption was promoted by BaP by activating the ROS‑driven NLRP3/caspase‑1 signaling pathway.</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"56 3","pages":""},"PeriodicalIF":5.7,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12236750/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144560123","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exosome‑mediated crosstalk between the cardiovascular and musculoskeletal systems: Mechanisms and therapeutic potential (Review).","authors":"Qingchen Li, Haoyang Gao, Xiaotong Ma, Ze Wang, Linlin Zhao, Weihua Xiao","doi":"10.3892/ijmm.2025.5570","DOIUrl":"10.3892/ijmm.2025.5570","url":null,"abstract":"<p><p>The cardiovascular and musculoskeletal systems are two core systems essential for maintaining human physiological functions and their dynamic interactions play a critical role in overall health. Exosomes, nanosized vesicles released by cells, contain bioactive substances including microRNA, long non‑coding RNA, lipids and proteins and participate in the pathophysiological regulation of multiple organ systems by mediating intercellular communication. Bone‑derived exosomes ameliorate cardiovascular diseases through the regulation of oxidative stress, inflammatory responses and apoptosis. Conversely, cardiovascular‑derived exosomes enhance bone homeostasis by suppressing osteoclast activity or promoting osteogenic differentiation, but they may also exacerbate pathological progression in conditions such as osteoarthritis. Skeletal muscle‑derived exosomes protect cardiomyocytes in muscular dystrophy through functional molecules delivery. However, under pathological conditions such as sarcopenia, skeletal muscle‑derived exosomes may aggravate cardiac dysfunction by activating pro‑apoptotic signals. Similarly, cardiovascular‑derived exosomes exhibit dual roles in skeletal muscle regulation, promoting regeneration while potentially inducing atrophy during heart failure. In addition, exosomes demonstrate significant clinical value as diagnostic biomarkers and targeted drug delivery vehicles, both for early disease detection and regenerative therapies. The present review systematically outlined the mechanisms underlying exosome‑mediated bidirectional crosstalk between the cardiovascular and musculoskeletal systems and explores their clinical application potential. It provided theoretical insights and novel perspectives for further research into the pathogenesis and therapeutic strategies of cardiovascular and musculoskeletal diseases.</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"56 3","pages":""},"PeriodicalIF":5.7,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12236749/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144505620","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"GW8510 alleviates muscle atrophy and skeletal muscle dysfunction in mice through AMPK/PGC1α signaling.","authors":"Yutong Chen, Zurui Liu, Chen Liu, Daqian Yang, Mengmeng Xiao, Zhengqian Li, Zhengwei Xie","doi":"10.3892/ijmm.2025.5569","DOIUrl":"10.3892/ijmm.2025.5569","url":null,"abstract":"<p><p>Preventing and restoring muscle loss and function is essential for elderly individuals. GW8510 may accelerate myotube differentiation. The present study aimed to investigate the protective effect of GW8510 (a CDK2 inhibitor) on muscle atrophy. Mouse models of muscle atrophy were induced by denervation, dexamethasone and glycerol. Muscle‑to‑body weight ratio, the cross‑sectional area of muscles, grip strength, fatigue and serum levels of superoxide dismutase and creatine kinase were assessed. <i>In vitro</i>, a dexamethasone‑induced C2C12 myotube atrophy model was used to evaluate mitochondrial function. Reverse transcription‑quantitative PCR, immunoblotting and small interfering RNA transfection were performed to explore the potential molecular mechanisms following treatment with GW8510. GW8510 resulted in a significant increase in the gastrocnemius and soleus muscle ratios in denervation mice (7 and 3%, respectively), alongside an increase in cross‑sectional area. Moreover, GW8510 significantly improved grip strength and superoxide dismutase activity, with similar protective effects in dexamethasone‑ and glycerol‑induced muscle atrophy models. GW8510 decreased reactive oxygen species production, increased mitochondrial DNA copy number, maintained mitochondrial dynamics and enhanced antioxidant activity in C2C12 myotubes. Mechanistically, GW8510 significantly inhibited the expression of atrophy‑associated markers F‑box protein 32 and tripartite motif‑containing 63 while activating AMPK (both P<0.01). The knockdown peroxisome proliferator‑activated receptor‑γ co‑activator‑1α (Pgc1α) negated the effects of GW8510. Overall, GW8510 mitigated muscle atrophy via the activation of the AMPK/PGC1α pathway. GW8510 could serve as a novel therapeutic agent for the prevention of muscle atrophy.</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"56 3","pages":""},"PeriodicalIF":5.7,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12236748/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144505621","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Advances of exosome regulating‑FXR to repair inflammatory bowel disease (Review).","authors":"Peter Muro, Caihong Jing, Yaru Qiao, Wenbing Wang, Bo Wang, Fei Mao","doi":"10.3892/ijmm.2025.5576","DOIUrl":"10.3892/ijmm.2025.5576","url":null,"abstract":"<p><p>Inflammatory bowel disease (IBD), which encompasses ulcerative colitis and Crohn's disease, poses significant treatment difficulties because of its persistent course and underlying inflammatory mechanisms. Existing treatments primarily focus on alleviating symptoms, while novel biological drugs that target specific molecular pathways could address the root causes of the disease. One such pathway involves the farnesoid X receptor (FXR), a nuclear receptor essential for bile acid metabolism, intestinal homeostasis and modulation of inflammation. Activating FXR can reduce intestinal inflammation and improve gut barrier function, highlighting its potential as a treatment target for IBD. However, using synthetic agonists to directly activate FXR has drawbacks, including off‑target effects and limited effectiveness. Exosomes, tiny nanoscale vesicles involved in cell‑to‑cell communication, have emerged as promising therapeutic tools for regulating FXR signaling in IBD. Exosomes, particularly those derived from mesenchymal stem cells, can deliver bioactive molecules that promote FXR activation, reduce inflammation, and enhance tissue regeneration. The present review examines how exosomes regulate FXR signaling and their potential therapeutic use in IBD. It covers exosome biogenesis, therapeutic benefits and their molecular mechanisms in IBD.</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"56 3","pages":""},"PeriodicalIF":5.7,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144560122","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Egr‑1 promotes the proliferation and migration of vascular smooth muscle cells by transcriptionally activating Egr‑2 in arteriovenous fistulas.","authors":"Ke Hu, Shichen Bu, Yi Guo, Yuxuan Li, Shiwen Yu, Lulu Wang, Chuanqi Cai, Yiqing Li, Xin Liu, Hegui Huang, Weici Wang","doi":"10.3892/ijmm.2025.5568","DOIUrl":"10.3892/ijmm.2025.5568","url":null,"abstract":"<p><p>Arteriovenous fistulas (AVFs) are preferred access points for hemodialysis. The present study aimed to investigate the function of early growth response‑1 (Egr‑1) in the proliferation and migration of smooth muscle cells (SMCs) and assess its potential as a new therapeutic target for AVF treatment. A comprehensive analysis combining public data‑source mining, human tissue collection, animal studies, cell culture experiments and various molecular biology techniques was conducted. The public dataset GSE119296 was used for immunohistochemical analyses of human AVF stenosis samples. SMC‑specific Egr‑1 knockout mice and various in vitro assays on primary rat vascular SMCs were used to evaluate the effect of Egr‑1 on the functional capacity of SMCs. RNA sequencing and chromatin immunoprecipitation sequencing was performed. Egr‑1 was upregulated in human AVF stenosis samples and cultured SMCs. Knockout of Egr‑1 in mice mitigated AVF outflow tract stenosis, improved flow dynamics and diminished neointima formation. <i>In vitro</i>, Egr‑1 ablation reduced SMC proliferation and migration; Egr‑1 transcriptionally activated Egr‑2. Increased Egr‑1 expression facilitated SMC proliferation and migration through Egr‑2 regulation, contributing to AVF stenosis. Consequently, targeting Egr‑1 may offer a novel therapeutic approach for managing AVF intimal hyperplasia and improving AVF patency and function in patients with end‑stage renal disease.</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"56 3","pages":""},"PeriodicalIF":5.7,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12215247/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144505619","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Microbiota metabolites affect sleep as drivers of brain‑gut communication (Review).","authors":"Hanxing Cheng, Wanying Yang, Huaiyi Xu, Wenwen Zhu, Ailin Gong, Xuemei Yang, Sen Li, Houping Xu","doi":"10.3892/ijmm.2025.5571","DOIUrl":"10.3892/ijmm.2025.5571","url":null,"abstract":"<p><p>Sleep plays a crucial role in maintaining and improving physical and mental health. However, the prevalence of sleep disorders is increasing in modern society. Recently, the gut‑brain axis has emerged as a prominent focus within the realm of sleep disorder research, with gut microbiota metabolites serving as essential factors in gut‑brain communication. The present study summarizes the emerging connections between gut microbiota metabolites and sleep, mainly focusing on those derived from tryptophan and dietary fiber metabolism. It discusses potential pathways and molecular processes by which sleep interacts with the gut microbiota metabolites, aiming to evaluate the feasibility of using gut microbiota interventions to treat sleep disorders.</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"56 3","pages":""},"PeriodicalIF":5.7,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12236747/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144560127","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}