Objective: In this research, we investigated the current status, hotspots, frontiers, and trends of research in the field of bone-tendon interface (BTI) from 2000 to 2023, based on bibliometrics and visualization and analysis in CiteSpace, VOSviewer, and a bibliometric package in R software.Methods: We collected and organized the papers in the Web of Science core collection (WoSCC) for the past 23 years (2000–2023), and extracted and analyzed the papers related to BTI. The extracted papers were bibliometrically analyzed using CiteSpace for overall publication trends, authors, countries/regions, journals, keywords, research hotspots, and frontiers.Results: A total of 1,995 papers met the inclusion criteria. The number of papers published and the number of citations in the field of BTI have continued to grow steadily over the past 23 years. In terms of research contribution, the United States leads in terms of the number and quality of publications, number of citations, and collaborations with other countries, while the United Kingdom and the Netherlands lead in terms of the average number of citations. The University of Leeds publishes the largest number of papers, and among the institutions hosting the 100 most cited papers Hospital for Special Surgery takes the top spot. MCGONAGLE D has published the highest number of papers (73) in the last 10 years. The top three clusters include #0 “psoriatic arthritis”, #1 “rotator cuff repair”, and #2 “tissue engineering”. The structure and function of the BTI and its key mechanisms in the healing process are the key to research, while new therapies such as mechanical stimulation, platelet-rich plasma, mesenchymal stem cells, and biological scaffolds are hot topics and trends in research.Conclusion: Over the past 23 years, global research on the BTI has expanded in both breadth and depth. The focus of research has shifted from studies concentrating on the structure of the BTI and the disease itself to new therapies such as biomaterial-based alternative treatments, mechanical stimulation, platelet-rich plasma, etc.

Acute kidney injury (AKI) is a clinical syndrome characterized by a rapid decline in renal function, high morbidity and mortality, and a lack of effective early diagnostic markers or targeted therapies. To address this critical unmet need, we employed an integrated multi-omics and network pharmacology approach to systematically investigate the molecular mechanisms and potential therapeutic targets of AKI. Core targets were identified through differential gene expression (DEG) analysis combined with weighted gene co-expression network analysis (WGCNA), followed by exploration using protein-protein interaction (PPI) networks and pathway enrichment analyses. Inflammation, oxidative stress, and energy metabolism emerged as key pathways involved in AKI pathogenesis. Using ten CytoHubba algorithms and the MCODE module for comprehensive screening, we identified three hub genes-ACO2, FBP1, and PFKL. Their expression patterns and cellular specificity were further characterized using single-cell RNA sequencing data from AKI renal tissues. Additionally, we constructed a miRNA-hub gene regulatory network, providing insights into miRNA-based therapeutic strategies. Molecular docking analysis identified three approved drugs-Ajmaline, Cimetidine, and Tretinoin-with strong binding affinities to the hub proteins, suggesting their potential for repurposing in AKI treatment. Finally, by reviewing knockout mouse models from the Mouse Genome Informatics (MGI) database and conducting in vitro cell experiments, we explored the in vivo and in vitro roles of these core targets, providing experimental evidence of their physiological relevance. Overall, this study integrates cross-cohort transcriptomic profiling, network-based hub prioritization, single-nucleus cell-type localization, translational drug repurposing analyses, and in vitro experimental validation thereby providing a multi-layered framework to prioritize candidate biomarkers for AKI.

Per- and polyfluoroalkyl substances (PFASs), particularly perfluorooctanoic acid (PFOA) and perfluorooctanesulfonic acid (PFOS), are persistent environment

Per- and polyfluoroalkyl substances (PFAS), particularly perfluorooctanoic acid (PFOA) and perfluorooctanesulfonic acid (PFOS), are persistent environmental pollutants with potential immunotoxic effects. Emerging epidemiological evidence suggests a link between PFAS exposure and autoimmune diseases, including rheumatoid arthritis (RA). However, the causal nature of this relationship remains unclear. Genetic instruments for circulating PFOA and PFOS levels were obtained from genome-wide association studies of European populations, while RA outcome data were sourced from the FinnGen consortium and United Kingdom Biobank. Associations were evaluated using multiple Mendelian randomization (MR) methods to assess the robustness of the findings. The inverse variance weighted method served as the primary approach. Additional methods, including MR-Egger, weighted median, simple mode, weighted mode, maximum likelihood estimation, and robust adjusted profile score, were applied to address potential pleiotropy and weak instrument bias. Sensitivity analyses, including Cochran Q -test for heterogeneity, MR-pleiotropy residual sum and outlier (MR-PRESSO) for pleiotropy detection, and leave-one-out analysis, were performed to validate the robustness of the findings. MR analysis identified a significant association between genetically predicted PFOA levels and increased RA risk (odds ratio = 1.87, 95% confidence interval [1.13–3.11], P = .015). Similarly, genetically predicted PFOS levels were positively associated with seropositive RA risk (odds ratio = 1.14, 95% confidence interval [1.00–1.29], P = .049). Sensitivity analyses confirmed the robustness of these findings, and reverse MR analysis did not indicate bidirectional causality. Our findings provide genetic evidence suggesting a potential association between PFAS exposure and RA risk. Given the widespread environmental persistence of PFAS, further investigation into potential health impacts and strategies to reduce exposure may be warranted. Further mechanistic studies are warranted to elucidate the biological pathways underlying the potential relationship between PFAS exposure and RA.

The therapeutic efficacy of immune checkpoint blockade is frequently compromised by the profound spatial heterogeneity of solid tumors, where distinct ecol