Naunyn-Schmiedeberg's archives of pharmacology最新文献

{"title":"Global hotspots and trends in AMPA receptor research (2000-2025): a bibliometric and visualization analysis.","authors":"Yunsheng Liu, Rongde Zhong, Xianlin Wu, Jinfang Zhang, Zengwei Kou","doi":"10.1007/s00210-025-04679-7","DOIUrl":"https://doi.org/10.1007/s00210-025-04679-7","url":null,"abstract":"<p><p>AMPA receptors (AMPARs) are critical excitatory ionotropic glutamate receptors involved in synaptic transmission, plasticity, and various neurological disorders. From 2000 to present (up to 2025), extensive research has explored their roles in brain function and disease, yet a comprehensive bibliometric analysis of this field is lacking. This study aims to provide a systematic bibliometric overview of AMPAR research from 2000 to present, identifying key trends, influential contributors, and emerging hotspots to guide future investigations. Data were retrieved from Web of Science, PubMed, and Scopus, encompassing 37,000 distinct publications. Bibliometric tools (CiteSpace, VOSviewer, and Bibliometrix) were employed to analyze publication trends, country/institution contributions, journal metrics, author productivity, and keyword clusters. The United States led in publication output (6,142 articles) and citations (410,626), followed by China and Japan. The Journal of Neuroscience and Neuron were the top journals, while Huganir RL was the most cited author. Research hotspots evolved from fundamental AMPAR properties (e.g., subunit composition) to disease associations (e.g., Alzheimer's, depression) and therapeutic strategies (e.g., AMPAR modulators). Keyword analysis revealed four themes: biochemical properties, physiological functions, pathological roles, and therapeutic targets. AMPAR research has transitioned from basic neurophysiology to translational applications, with growing emphasis on neurological and psychiatric disorders. Future directions include elucidating native AMPAR complexes, trafficking dynamics, and precision therapeutics. This study highlights the field's progression and underscores the need for interdisciplinary collaboration to address unresolved challenges.</p>","PeriodicalId":18876,"journal":{"name":"Naunyn-Schmiedeberg's archives of pharmacology","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2025-10-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145275386","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Elevated PXDC1 expression linked to poor prognosis and abnormalities in PD-L1 regulation and NK cell function in colorectal cancer.","authors":"Wei Cheng, Di Gao, Junyu Ren, Jiaxin Liu","doi":"10.1007/s00210-025-04628-4","DOIUrl":"https://doi.org/10.1007/s00210-025-04628-4","url":null,"abstract":"<p><p>Colorectal cancer (CRC) remains a prevalent malignancy with suboptimal treatment outcomes, underscoring the need for novel prognostic and therapeutic biomarkers. This research is the initial exploration into the role of PXDC1 in CRC, analyzing its differential expression, prognostic significance, and correlation with tumor-infiltrating immune cells through transcriptomics, spatial transcriptomics, and single-cell genomics. Immunohistochemistry (IHC) staining confirmed that PXDC1 expression was notably higher in CRC tissues compared to normal tissues, highlighting its potential role in CRC progression. Functional assays, including CCK8, colony formation, scratch assays, and flow cytometry, showed that PXDC1 knockdown in CRC cells inhibited proliferation, migration, and induced apoptosis. Additional analyses utilizing bioinformatics, Western blotting, co-culture experiments, molecular docking, and immunofluorescence revealed a positive correlation between PXDC1 and PD-L1 expression. Knockdown of PXDC1 enhanced the tumor-killing capacity of NK-92 cells and promoted increased cytokine release. These results indicate that PXDC1 is pivotal in CRC progression, where its elevated levels are linked to poor prognosis, tumor growth, immune cell infiltration, and NK cell impairment. This highlights PXDC1's potential as a significant prognostic biomarker and an attractive therapeutic target for CRC, offering opportunities for more precise and targeted treatment approaches.</p>","PeriodicalId":18876,"journal":{"name":"Naunyn-Schmiedeberg's archives of pharmacology","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2025-10-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145275313","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The publish or perish, publish and perish, publish then perish, and now retract and perish cultures in academia.","authors":"Jaime A Teixeira da Silva, Serhii Nazarovets","doi":"10.1007/s00210-025-04651-5","DOIUrl":"https://doi.org/10.1007/s00210-025-04651-5","url":null,"abstract":"<p><p>The publish-or-perish (POP) culture in academic publishing has become ingrained for several reasons and may be a phenomenon that is difficult to erase simply because publishing remains the most visible form of recognition for scientists, who use both publishing and the recognition it confers to remain relevant while securing their status, employment, funding, visibility, and other benefits. Although scientific publishing has immeasurable benefits when it represents thoroughly conducted research or an integrated philosophy, when observed through the prism of POP culture, a negative connotation is associated with it. As the POP adage implies, if one does not publish, then one may figuratively and intellectually perish (i.e., publish and perish), and when this transcends to a literal plane, the adage publish then perish is born. At a more extreme level, and no longer driven by the desire to publish, the retraction of intellect or literature due to error or misconduct has diversified POP culture by adding a layered adage of retract and perish, where the latter may occur both figuratively and literally. In this essay, an attempt is made to identify several factors that may induce POP culture and the impact it has on individual careers, knowledge creation, the benevolence of scientific endeavor, and the well-being of science, society, and Humanity.</p>","PeriodicalId":18876,"journal":{"name":"Naunyn-Schmiedeberg's archives of pharmacology","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2025-10-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145274960","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The immunoregulatory role of lncRNA UCA1: a pan-cancer perspective with a focus on colorectal cancer.","authors":"Fatemeh Maghool, Parisa Kadkhodaei Elyaderani, Ahmadreza Rajabi, Fatemeh Balangi, Aida Heidari, Samane Mohammadzadeh, Mohammad Hassan Emami, Pouria Samadi","doi":"10.1007/s00210-025-04588-9","DOIUrl":"https://doi.org/10.1007/s00210-025-04588-9","url":null,"abstract":"<p><p>Long non-coding RNA UCA1 has emerged as a critical regulator in cancer biology. This study comprehensively investigates UCA1 expression and its functional relevance across multiple cancer types, with a focus on colorectal cancer (CRC). Pan-cancer analyses were conducted using data retrieved from TCGA, GTEx, cBioPortal, and BEST databases, integrated via R programming. Single-cell RNA sequencing data from CellxGene platform were used to explore cell-type-specific UCA1 expression. Functional enrichment, co-expression networks, genomic alterations, diagnostic profile, CpG methylation, immune associations, and drug response profiles as well as experimental validation were also assessed. UCA1 was significantly overexpressed in at least 10 tumor types, most notably in CRC. Single-cell analysis revealed UCA1 expression across epithelial, stromal, and immune cell populations, including T cells and plasma cells. UCA1 correlated with genes like GRHL3 and KLK8, implicating roles in tissue development, adhesion, and motility. Genomic analyses revealed copy number amplifications (e.g., 17q12) and altered methylation patterns. Elevated UCA1 expression was linked to poorer prognosis in several cancers and positively correlated with recurrence and progression risk in CRC and other tumors. Immune analysis showed UCA1's association with regulatory T cells, chemokines, and immune checkpoints, indicating an immunosuppressive role. Additionally, UCA1 impacted drug resistance and sensitivity across therapies. UCA1 plays a multifaceted role in cancer progression, immune modulation, and therapy response. Its expression in diverse cell types within the tumor microenvironment and association with clinical outcomes supports its potential as a prognostic biomarker and therapeutic target, especially in CRC.</p>","PeriodicalId":18876,"journal":{"name":"Naunyn-Schmiedeberg's archives of pharmacology","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2025-10-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145274992","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Fabrication of nogalamycin-loaded zeolitic imidazolate framework-8 metal-organic frameworks for promising drug carrier for lung cancer and antibacterial treatment.","authors":"Yaser E Alqurashi, Faiz Abdulaziz Alfaiz, Mickymaray Suresh","doi":"10.1007/s00210-025-04673-z","DOIUrl":"https://doi.org/10.1007/s00210-025-04673-z","url":null,"abstract":"<p><p>Lung cancer is a major malignant neoplasm, and nogalamycin (NAM) is among the most often utilized drug agents in its treatment. Due to nogalamycin's unfavorable characteristics and adverse consequences, nano-drug delivery methods are under development. ZIF-8, a metal-organic framework (MOF), provides an optimal platform for drug release and delivery owing to its pH-sensitive and Zn²⁺ composition biodegradable properties. The current work achieved encapsulation of nogalamycin in ZIF-8 with an efficiency of 53.8% and a loading capacity of 58% (NAM@ZIF-8). The structural characteristics of the newly developed NAM@ZIF-8 systems were examined. The NAM release study demonstrated a more rapid release pattern at pH = 5.0 than at pH = 7.4. The anticancer properties of nogalamycin and Zn²⁺ were investigated in vitro using H1299 and A549 cells. The findings indicated that, alongside nogalamycin, ZIF-8 contributed Zn²⁺ to the milieu through its biodegradable assembly, resulting in a significant anticancer effect on lung cancer cell lines. In addition, the NAM@ZIF-8 NPs displayed excellent antibacterial activity against Escherichia coli and Staphylococcus aureus. Further, the release of NAM from NAM@ZIF-8 NPs resulted in the continuous release of antibacterial activities. The results indicated that formulations incorporating Zn²⁺ and nogalamycin were more efficacious in treating lung cancer and antibacterial than nogalamycin alone.</p>","PeriodicalId":18876,"journal":{"name":"Naunyn-Schmiedeberg's archives of pharmacology","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2025-10-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145275345","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Fucoidan induces ferroptosis in colorectal cancer cells by regulating the SLC7A11/GPX4 signaling pathway and modulating metabolic pathways.","authors":"Chengyu Yang, Chunqi Feng, Naiqi Zhang, Jia Feng, Shulian Xie, Xinghua Li, Qi Liu","doi":"10.1007/s00210-025-04698-4","DOIUrl":"https://doi.org/10.1007/s00210-025-04698-4","url":null,"abstract":"<p><strong>Objective: </strong>This study investigates the impact of fucoidan on ferroptosis in colorectal cancer (CRC) cells and analyzes its mechanism of action through the SLC7A11/GPX4 signaling pathway.</p><p><strong>Methods: </strong>The HT-29 colorectal cancer cell line was tested using the CCK-8 cytotoxicity assay to assess how different fucoidan concentrations affect cell survival, and the IC₅₀ value was determined. Cell proliferation was evaluated using the colony formation assay, and the ability of cell migration was assessed using both the scratch test and transwell assay. The relative levels of ferrous ion (Fe²⁺), malondialdehyde (MDA), and glutathione (GSH) in the cells were quantified using kits for ferrous ion, MDA, and GSH. Ferroptosis-related gene expression at the mRNA level was identified through qRT-PCR. The levels of proteins related to ferroptosis, including SLC7A11, GPX4, and COX2, were assessed through Western blot. Employs ultra performance liquid chromatography-mass spectrometry (UPLC-MS) to measure the levels of endogenous metabolites within cells, identify potential differential metabolites, and analyze their associated metabolic pathways.</p><p><strong>Results: </strong>The results of the CCK-8 assay, colony formation assay, scratch assay and Transwell assay indicated that fucoidan significantly inhibited the proliferation and migration of HT-29 cells (P < 0.01). The results of Fe²⁺, MDA and GSH detection showed that fucoidan was able to raise the levels of Fe²⁺ and MDA (P < 0.01) while reducing GSH (P < 0.01) in HT-29 cells. Further examination using qRT-PCR and Western blot analysis indicated that fucoidan upregulates COX2 mRNA and protein expression while significantly decreasing the levels of SLC7A11 and GPX4 mRNA and protein (P < 0.05, P < 0.01). The results of the metabolomics analysis demonstrate that fucoidan significantly modulates 27 potential differential metabolites. Additionally, an enrichment analysis of the key metabolites influenced by fucoidan indicates that it primarily impacts metabolic pathways such as phenylalanine metabolism, glycerophospholipid metabolism and sphingolipid metabolism.</p><p><strong>Conclusion: </strong>Fucoidan induces ferroptosis in colorectal cancer cells, potentially through the regulation of the SLC7A11/GPX4 signaling pathway and associated metabolic pathways, including amino acid and lipid metabolism.</p>","PeriodicalId":18876,"journal":{"name":"Naunyn-Schmiedeberg's archives of pharmacology","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2025-10-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145275340","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Vulvovaginal candidiasis in rural pregnant populations from Uttar Pradesh, India: species shift, biofilm formation, and resistance trends.","authors":"Soha Abdallah Moursi, Rashmi Saxena, Fareya Haider, Mohd Shahid Khan, Mohd Saleem, Irfan Ahmad, Nadeem Ahmad","doi":"10.1007/s00210-025-04699-3","DOIUrl":"https://doi.org/10.1007/s00210-025-04699-3","url":null,"abstract":"<p><p>Vulvovaginal candidiasis (VVC) is a common infection in pregnancy, with increasing concern over the emergence of non-albicans Candida (NAC) species and antifungal resistance, particularly in biofilm-forming strains. A total of 913 pregnant women with clinically suspected VVC were evaluated. Demographic and clinical data were collected, and specimens were processed using KOH mount and fungal culture. Isolates were identified to the species level using matrix-assisted laser desorption ionization time-of-flight mass spectrometry (MALDI-TOF MS), assessed for biofilm formation by the tissue culture plate (TCP) method, and tested for antifungal susceptibility by Kirby-Bauer disk diffusion method. The highest prevalence was observed in women aged 23-28 years (35.7%) and those from rural areas (61.7%). Illiteracy (54.5%), third-trimester pregnancy (43.7%), and multigravida status (57.6%) were predominant. Mixed symptoms, especially the triad of itching, burning, and discharge (27.2%), were most common. Culture had a higher sensitivity (83.6%) than KOH microscopy (77.2%). Candida albicans was the predominant species (59.8%), followed by Candida glabrata (15.3%) and Candida tropicalis (9.8%). NAC species accounted for 40.2% of isolates. Biofilm production was highest in C. albicans (85.1%), C. tropicalis (74.7%), and C. glabrata (59.8%). Antifungal resistance was significantly higher in biofilm producers, particularly to azoles: ketoconazole (83.3% vs. 16.7%, p < 0.001) and fluconazole (81.5% vs. 18.5%, p < 0.001). Amphotericin B also showed reduced efficacy in biofilm producers (66.7% vs. 33.3%, p < 0.05). This study reports a high prevalence of VVC (83.6%) in pregnant women, predominantly in rural, less-educated, and multigravida groups. C. albicans remained the leading pathogen, but the notable presence of non-albicans species reflects a shifting epidemiology. Biofilm formation, especially by C. albicans, C. tropicalis, and C. glabrata, correlated with marked azole resistance. Routine species-level identification, biofilm evaluation, and antifungal susceptibility testing are essential for optimizing treatment in pregnancy.</p>","PeriodicalId":18876,"journal":{"name":"Naunyn-Schmiedeberg's archives of pharmacology","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2025-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145251927","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Systematic investigation of the potential multi-target pharmacological mechanisms of Astragaloside IV in polycystic ovary syndrome via network pharmacology and in vivo/in vitro experiments.","authors":"Ying Feng, Lei Wu, Jianrong Liu","doi":"10.1007/s00210-025-04667-x","DOIUrl":"https://doi.org/10.1007/s00210-025-04667-x","url":null,"abstract":"<p><p>Polycystic ovary syndrome (PCOS) is a prevalent endocrine-metabolic disorder affecting reproductive-aged women and is characterized by hyperandrogenemia, ovulatory dysfunction, and polycystic ovaries. Astragaloside IV (AS-IV), an active compound derived from Astragalus membranaceus, shows promise in the treatment of metabolic disorders. However, the precise molecular targets and mechanisms of action in PCOS remain unclear. This study aimed to elucidate the therapeutic effects and underlying mechanisms of AS-IV in PCOS. AS-IV's therapeutic effects of AS-IV were assessed in a rat model of PCOS. Potential AS-IV targets were predicted using the PharmMapper and SwissTargetPrediction databases and expanded using STRINGdb. PCOS-related differentially expressed genes (DEGs) were identified from Gene Expression Omnibus (GEO)datasets, and weighted gene co-expression network analysis (WGCNA) revealed the disease-associated gene modules. Overlapping drug-disease targets were analyzed using protein-protein interaction (PPI) network, Gene Ontology (GO), and KEGG pathway enrichment. The core targets were validated using molecular docking. In vitro, qPCR was used to assess key gene expression in the control, DHT model, AS-IV, EP300 inhibitor (C646), and Nrf2 inhibitor (ML385) groups. A total of 371 potential AS-IV targets were identified. Analysis of GEO data yielded 2286 DEGs, with WGCNA identifying key PCOS-related modules and hub genes. The intersection revealed 31 key targets, including five core genes. In vivo, AS-IV improved ovarian pathology, increased antioxidant enzyme levels, reduced inflammatory cytokine, testosterone, and LH levels, and increased estradiol levels. In vitro, the PCOS, EP300, and Nrf2 inhibitor groups showed decreased EP300, NFE2L2, HMOX1, and AKT1 expression and increased MMP9 expression compared to the controls and AS-IV group. AS-IV ameliorated endocrine and ovarian abnormalities in PCOS by modulating the EP300/Nrf2/HMOX1/MMP9 axis, demonstrating multi-target antioxidant, anti-inflammatory, and hormone-regulatory effects, supporting its potential as a therapeutic agent for PCOS.</p>","PeriodicalId":18876,"journal":{"name":"Naunyn-Schmiedeberg's archives of pharmacology","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2025-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145251933","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Truncated pardaxin derivative D18.13 induces selective breast cancer apoptosis via predicted targeting of MAPK8.","authors":"Yong Hui Wong, Hao Dong Tan, Yin Sim Tor, Phelim Voon Chen Yong, Sau Har Lee","doi":"10.1007/s00210-025-04671-1","DOIUrl":"https://doi.org/10.1007/s00210-025-04671-1","url":null,"abstract":"<p><p>Cancer remains a global health issue, whereby the adverse effects of conventional drugs urge the discovery of modalities for replacement, such as anticancer peptides with higher selectivity against cancer cells. Bioactive peptide pardaxin has anticancer effects, but its concurrent haemolytic effects possess limitations. This study aimed to discover shortened pardaxin derivatives using in silico analyses, followed by the study of their cytotoxic effects on breast cancer and normal cells. Pardaxin was truncated to 27 or 18 residues, and then single residue replacement was induced using AntiCP 2.0. The generated sequences were further predicted to identify potential derivatives with anticancer, non-toxic, low haemolysis, conserved alpha-helices structure, and stronger docking affinity towards FAS death receptor. Synthesised potential derivatives were validated using MTT assay on breast cancer and normal cells, haemolytic assay, FITC-Annexin V binding, and lactate dehydrogenase (LDH) assay for apoptosis and necrosis investigation. Potential targets in the MAPK/JNK pathway to induce apoptosis were determined using HDOCK docking screening and validated via molecular dynamics (MD) simulation and MM/GBSA calculation. Among the synthesised peptides, D18.13 demonstrated the highest potential due to its breast cancer-killing ability, lowest toxicity on normal cells, and with alleviated haemolytic effects. The D18.13-treated breast cancer cells showed remarkable apoptotic effects. The D18.13 potentially targets MAPK8 to induce MAPK/JNK-mediated apoptosis, with MM/GBSA revealing a free binding energy (-67.40 kcal/mol) similar to that of parental pardaxin (-68.88 kcal/mol). The in silico method enhanced anticancer peptide discovery such as D18.13, which has the potential to treat breast cancer with minimal side effects.</p>","PeriodicalId":18876,"journal":{"name":"Naunyn-Schmiedeberg's archives of pharmacology","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2025-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145251962","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Assessing the disease burden of opioid use disorder in western europe: trends, gender differences, and future directions.","authors":"Dingwen Xu, Rui Zhang, Jingjing Li, Jijun Wu, Zhe Yang","doi":"10.1007/s00210-025-04657-z","DOIUrl":"https://doi.org/10.1007/s00210-025-04657-z","url":null,"abstract":"<p><p>Opioid Use Disorder (OUD) has emerged as a significant public health challenge worldwide, and the issue of OUD in Western Europe is equally severe. However, there is a lack of systematic analyses specifically focusing on OUD in Western Europe, with existing research primarily concentrated in North America. This limitation hampers our understanding of the true burden of OUD in Western Europe. This study aims to fill the gap in research regarding the burden of OUD in Western Europe by analyzing the epidemiological characteristics from 1990 to 2021. It seeks to provide a comprehensive assessment of the disease burden in the region and to offer scientific evidence for policy-making. The study is based on data from the Global Burden of Disease (GBD) 2021, utilizing the publicly available database from the Institute for Health Metrics and Evaluation (IHME). It analyzes indicators such as incidence, prevalence, mortality, and Disability-Adjusted Life Years (DALYs) across Western European countries. The study employs the Estimated Annual Percentage Change (EAPC) to analyze trends and uses the Autoregressive Integrated Moving Average (ARIMA) model to predict the changes in OUD over the next fifteen years. The analysis reveals that the burden of OUD in Western Europe is generally high across all age groups, particularly among those aged 15 to 60. The burden is significantly higher in males than in females, although the rate of increase is faster among females. Between 1990 and 2021, both mortality rates and years lost to disability have increased significantly, with notable growth in the disease burden in certain countries such as Sweden and the United Kingdom. The ARIMA model predicts that the overall burden of OUD in Western Europe will continue to exceed global levels by 2036, with significant variations in trend patterns among individual countries. This study reveals the complex epidemiological characteristics and future trends of OUD in Western Europe, providing important evidence for the development of targeted prevention and intervention strategies. By identifying high-risk populations and key intervention areas, resource allocation can be optimized, enhancing the effectiveness of interventions to effectively address the opioid crisis.</p>","PeriodicalId":18876,"journal":{"name":"Naunyn-Schmiedeberg's archives of pharmacology","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2025-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145251930","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}