Bone & Joint Research最新文献

{"title":"Erratum.","authors":"Yan Xiao, Zhang Yue, He Zijing, Zheng Yao, Mao Sui, Zeng Xuemin, Zhang Qiang, Yuan Xiao, Ren Dapeng","doi":"10.1302/2046-3758.143.BJR-2025-00003","DOIUrl":"10.1302/2046-3758.143.BJR-2025-00003","url":null,"abstract":"","PeriodicalId":9074,"journal":{"name":"Bone & Joint Research","volume":"14 3","pages":"223"},"PeriodicalIF":4.7,"publicationDate":"2025-03-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11904850/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143613258","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Identification and validation of transcriptome-wide association study-derived genes as potential druggable targets for osteoarthritis.","authors":"Xindie Zhou, Xinjian Ye, Jiapei Yao, Xiaolong Lin, Yiping Weng, Yong Huang, Yaojun Lu, JingJing Shang, Luming Nong","doi":"10.1302/2046-3758.143.BJR-2024-0251.R1","DOIUrl":"10.1302/2046-3758.143.BJR-2024-0251.R1","url":null,"abstract":"<p><strong>Aims: </strong>Osteoarthritis (OA) is a widespread chronic degenerative joint disease with an increasing global impact. The pathogenesis of OA involves complex interactions between genetic and environmental factors. Despite this, the specific genetic mechanisms underlying OA remain only partially understood, hindering the development of targeted therapeutic strategies.</p><p><strong>Methods: </strong>A transcriptome-wide association study (TWAS) was conducted for site-specific OA phenotypes using functional summary-based imputation (FUSION). High-confidence candidate genes were identified through rigorous quality control measures, including joint/conditional analysis, permutation tests, best model evaluation, and colocalization analysis. Co-expression network analysis was performed to elucidate the functional biology of these candidate genes. Druggable gene targets and their structural models were retrieved from the DrugBank and SWISS-MODEL databases. Finally, the enrichment of mitogen-activated protein kinase 3 (<i>MAPK3</i>) and <i>SMAD3</i> in OA was validated biochemically using in vitro and in vivo OA models, as well as human histological sections.</p><p><strong>Results: </strong>Utilizing the FUSION algorithm, TWAS identified 794 candidate genes for OA. After quality control, 14 genes were classified as high-confidence genes, with seven recognized as potential drug targets including <i>GCAT, MAPK3, MST1R, PFKM, RAD9A, SMAD3,</i> and <i>USAP8</i>. Co-expression analysis revealed a strong biological association between <i>SMAD3</i> and <i>MAPK3</i>. Both in vitro and in vivo experiments demonstrated high activity and enriched expression of these two genes in OA.</p><p><strong>Conclusion: </strong>The present study identified tissue-specific candidate genes and validated high-confidence druggable targets for OA, providing new insights into the genetic landscape and biological processes involved in OA. Further functional studies are warranted to confirm these findings.</p>","PeriodicalId":9074,"journal":{"name":"Bone & Joint Research","volume":"14 3","pages":"224-235"},"PeriodicalIF":4.7,"publicationDate":"2025-03-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11904851/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143613261","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mechanical compression induces chondrocyte hypertrophy by regulating Runx2 O-GlcNAcylation during temporomandibular joint condyle degeneration.","authors":"Yan Xiao, Zhang Yue, He Zijing, Zheng Yao, Mao Sui, Zeng Xuemin, Zhang Qiang, Yuan Xiao, Ren Dapeng","doi":"10.1302/2046-3758.143.BJR-2024-0257.R1","DOIUrl":"10.1302/2046-3758.143.BJR-2024-0257.R1","url":null,"abstract":"<p><strong>Aims: </strong>Excessive chondrocyte hypertrophy is a common feature in cartilage degeneration which is susceptible to joint overloading, but the relationship between mechanical overloading and chondrocyte hypertrophy still remains elusive. The aim of our study was to explore the mechanism of mechanical compression-induced chondrocyte hypertrophy.</p><p><strong>Methods: </strong>In this study, the temporomandibular joint (TMJ) degeneration model was built through forced mandibular retrusion (FMR)-induced compression in TMJ. Chondrocytes were also mechanically compressed in vitro. The role of O-GlcNAcylation in mechanical compression-induced chondrocyte hypertrophy manifested through specific activator Thiamet G and inhibitor OSMI-1.</p><p><strong>Results: </strong>Both in vivo and in vitro data revealed that chondrocyte hypertrophic differentiation is promoted by compression. Immunofluorescent and immunoblotting results showed that protein pan-O-GlcNAcylation levels were elevated in these hypertrophic chondrocytes. Pharmacologically inhibiting protein pan-O-GlcNAcylation by OSMI-1 partially mitigated the compression-induced hypertrophic differentiation of chondrocytes. Specifically, runt-related transcription factor 2 (Runx2) and SRY-Box 9 transcription factor (Sox9) were subjected to modification of O-GlcNAcylation under mechanical compression, and pharmacological activation or inhibition of O-GlcNAcylation affected the transcriptional activity of Runx2 but not Sox9. Furthermore, compression-induced protein pan-O-GlcNAcylation in chondrocytes was induced by enhanced expression of glucose transporter 1 (GLUT1), and depletion of GLUT1 by WZB117 dampened the effect of compression on chondrocyte hypertrophy.</p><p><strong>Conclusion: </strong>Our study proposes a novel function of GLUT1-mediated protein O-GlcNAcylation in driving compression-induced hypertrophic differentiation of chondrocytes by O-GlcNAc modification of Runx2, which promoted its transcriptional activity and strengthened the expressions of downstream hypertrophic marker.</p>","PeriodicalId":9074,"journal":{"name":"Bone & Joint Research","volume":"14 3","pages":"209-222"},"PeriodicalIF":4.7,"publicationDate":"2025-03-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11890221/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143584595","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Corrigendum.","authors":"Yayuan Guo, Xueliang Peng, Bin Cao, Qian Liu, Shen Li, Fulin Chen, Dalong Zhi, Shequn Zhang, Zhuoyue Chen","doi":"10.1302/2046-3758.143.BJR-2025-00002","DOIUrl":"10.1302/2046-3758.143.BJR-2025-00002","url":null,"abstract":"","PeriodicalId":9074,"journal":{"name":"Bone & Joint Research","volume":"14 3","pages":"208"},"PeriodicalIF":4.7,"publicationDate":"2025-03-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11881868/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143555427","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Aberrant anabolism hinders constructive metabolism of chondrocytes by pharmacotherapy in osteoarthritis.","authors":"Raquel Largo, Aranzazu Mediero, Cristina Villa-Gomez, Ismael Bermejo-Alvarez, Gabriel Herrero-Beaumont","doi":"10.1302/2046-3758.143.BJR-2024-0241.R1","DOIUrl":"10.1302/2046-3758.143.BJR-2024-0241.R1","url":null,"abstract":"<p><p>Osteoarthritis (OA) is a highly prevalent and disabling disease with an unmet therapeutic need. The characteristic cartilage loss and alteration of other joint structures result from a complex interaction of multiple risk factors, with mechanical overload consistently playing a central role. This overload generates an inflammatory response in the cartilage due to the activation of the innate immune response in chondrocytes, which occurs through various cellular mechanisms. Moreover, risk factors associated with obesity, being overweight, and metabolic syndrome enhance the inflammatory response both locally and systemically. OA chondrocytes, the only cells present in articular cartilage, are therefore inflamed and initiate an anabolic process in an attempt to repair the damaged tissue, which ultimately results in an aberrant and dysfunctional process. Under these circumstances, where the cartilage continues to be subjected to chronic mechanical stress, proposing a treatment that stimulates the chondrocytes' anabolic response to restore tissue structure does not appear to be a therapeutic target with a high likelihood of success. In fact, anabolic drugs proposed for the treatment of OA have yet to demonstrate efficacy. By contrast, multiple therapeutic strategies focused on pharmacologically managing the inflammatory component, both at the joint and systemic levels, have shown promise. Therefore, prioritizing the control of chronic innate pro-inflammatory pathways presents the most viable and promising therapeutic strategy for the effective management of OA. As research continues, this approach may offer the best opportunity to alleviate the burden of this incapacitating disease.</p>","PeriodicalId":9074,"journal":{"name":"Bone & Joint Research","volume":"14 3","pages":"199-207"},"PeriodicalIF":4.7,"publicationDate":"2025-03-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11881514/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143555444","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The role of AGEs in muscle ageing and sarcopenia.","authors":"Zhaojing Guo, Hengzhen Li, Shide Jiang, Masoud Rahmati, Jingyue Su, Shengwu Yang, Yuxiang Wu, Yusheng Li, Zhenhan Deng","doi":"10.1302/2046-3758.143.BJR-2024-0252.R1","DOIUrl":"10.1302/2046-3758.143.BJR-2024-0252.R1","url":null,"abstract":"<p><p>Sarcopenia is an ageing-related disease featured by the loss of skeletal muscle quality and function. Advanced glycation end-products (AGEs) are a complex set of modified proteins or lipids by non-enzymatic glycosylation and oxidation. The formation of AGEs is irreversible, and they accumulate in tissues with increasing age. Currently, AGEs, as a biomarker of ageing, are viewed as a risk factor for sarcopenia. AGE accumulation could cause harmful effects in the human body such as elevated inflammation levels, enhanced oxidative stress, and targeted glycosylation of proteins inside and outside the cells. Several studies have illustrated the pathogenic role of AGEs in sarcopenia, which includes promoting skeletal muscle atrophy, impairing muscle regeneration, disrupting the normal structure of skeletal muscle extracellular matrix, and contributing to neuromuscular junction lesion and vascular disorders. This article reviews studies focused on the pathogenic role of AGEs in sarcopenia and the potential mechanisms of the detrimental effects, aiming to provide new insights into the pathogenesis of sarcopenia and develop novel methods for the prevention and therapy of sarcopenia.</p>","PeriodicalId":9074,"journal":{"name":"Bone & Joint Research","volume":"14 3","pages":"185-198"},"PeriodicalIF":4.7,"publicationDate":"2025-03-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11878473/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143555673","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Development of a novel rat long-bone nonunion model and efficacy evaluation of a prostaglandin EP4 selective agonist (AKDS001) combined with iliac bone grafting.","authors":"Daisuke Tateiwa, Masahiro Nishida, Joe Kodama, Hiromasa Hirai, Shinichi Nakagawa, Yuichiro Ukon, Kazuhiro Takeyama, Natsumi Yamamori, Kyoko Hirano, Masato Ikuta, Takayuki Kitahara, Takuya Furuichi, Masayuki Bun, Seiji Okada, Takashi Kaito","doi":"10.1302/2046-3758.143.BJR-2024-0220.R1","DOIUrl":"10.1302/2046-3758.143.BJR-2024-0220.R1","url":null,"abstract":"<p><strong>Aims: </strong>Nonunion occurs when a fracture fails to heal permanently, often necessitating surgical intervention to stimulate the bone healing response. Current animal models of long-bone nonunion do not adequately replicate human pathological conditions. This study was intended as a preliminary investigation of a novel rat nonunion model using a two-stage surgical intervention, and to evaluate the efficacy of a selective prostaglandin E2 receptor 4 agonist (AKDS001) as a novel nonunion therapeutic agent compared with existing treatments.</p><p><strong>Methods: </strong>Initially, Sprague-Dawley rats underwent intramedullary Kirschner wire (K-wire) fixation of a femoral fracture with the interposition of a 2 mm-thick silicon disc. After three weeks, the silicon disc was removed, and the intramedullary K-wire was replaced with plate fixation while maintaining the 2 mm defect. Contrary to the control group (1) that received no treatment, the following therapeutic interventions were performed at injury sites after freshening: (2) freshening group: no grafting; (3) iliac bone (IB) group: IB grafting; (4) AKDS group: AKDS001-loaded microspheres (MS) combined with IB (0.75 mg/ml); and (5) bone morphogenetic protein (BMP) group: grafting of a BMP-2-loaded collagen sponge (10 μg; 0.10 mg/ml). After six weeks, micro-CT (μCT) and histological analysis was performed.</p><p><strong>Results: </strong>In the control group, the radiological union rate was 0%, and histological findings showed that fracture sites comprised fibrous scar tissue, resembling the histology of human nonunion. The union rates in the freshening, IB, AKDS, and BMP groups were 16.7%, 0%, 62.5%, and 50.0%, respectively. The AKDS group demonstrated a significantly higher union rate than the IB group (p = 0.026). μCT and histological analysis indicated that the quality of newly formed bone was superior in the AKDS group than in the BMP group.</p><p><strong>Conclusion: </strong>We developed a novel long-bone nonunion model. The co-therapy of AKDS001-MS and IB grafting presents a promising new treatment for nonunion.</p>","PeriodicalId":9074,"journal":{"name":"Bone & Joint Research","volume":"14 3","pages":"166-175"},"PeriodicalIF":4.7,"publicationDate":"2025-03-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11873957/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143540079","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Rapid multiplex micro-ELISA assay for simultaneous measurement of synovial biomarkers : a potential aid in diagnosing periprosthetic joint infection?","authors":"Martina Maritati, Michael Vogl, Max Sonnleitner, Andrej Trampuz","doi":"10.1302/2046-3758.143.BJR-2024-0100.R1","DOIUrl":"10.1302/2046-3758.143.BJR-2024-0100.R1","url":null,"abstract":"<p><strong>Aims: </strong>The diagnosis of periprosthetic joint infection (PJI) remains a challenge, as no single diagnostic test shows high diagnostic accuracy. Recently, the measurement of synovial biomarkers has shown promising results. The aim of this study was to present a novel multiplex micro-enzyme-linked immunosorbent assay (ELISA) method for the rapid and simultaneous measurement of alpha-defensin, interleukin (IL)-6, and calprotectin developed in a model buffer system and human spiked synovial fluid.</p><p><strong>Methods: </strong>A microfluidics- and chemiluminescence-based multiplex micro-ELISA point-of-care testing system was employed for the rapid and simultaneous measurement of alpha-defensin, calprotectin, and IL-6 developed in a model buffer system and spiked human synovial fluid. Cut-off values of 1.56 µg/ml for alpha-defensin, 50 µg/ml for calprotectin, and 0.031 µg/ml for IL-6 were extracted from the literature as optimal cut-off values for the diagnosis of PJI, and were used for comparison.</p><p><strong>Results: </strong>Limit of detection (LoD) was determined for each individual biomarker by means of calibration curves with serial dilutions in a model buffer system. LoDs of 0.008, 0.002, and 0.00014 µg/ml were determined for alpha-defensin, calprotectin, and IL-6, respectively. The spiked synovial fluid assay determined LoDs of 0.08, 0.31, and 0.004 µg/ml for alpha-defensin, calprotectin, and IL-6, respectively.</p><p><strong>Conclusion: </strong>These findings highlight the proposed platform's unique features, including simultaneous measurement of three key synovial biomarkers, minimal sample volume requirements (5 to 50 µl), lower LoDs compared to conventional tests, and a short processing turnaround time of 22 minutes. Further validation studies are necessary to confirm its clinical utility.</p>","PeriodicalId":9074,"journal":{"name":"Bone & Joint Research","volume":"14 3","pages":"176-184"},"PeriodicalIF":4.7,"publicationDate":"2025-03-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11874355/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143540080","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A bilayer scaffold of collagen and nanohydroxyapatite promotes osteochondral defect in rabbit knee joints.","authors":"Yayuan Guo, Xueliang Peng, Bin Cao, Qian Liu, Shen Li, Fulin Chen, Dalong Zhi, Shequn Zhang, Zhuoyue Chen","doi":"10.1302/2046-3758.142.BJR-2024-0171.R1","DOIUrl":"10.1302/2046-3758.142.BJR-2024-0171.R1","url":null,"abstract":"<p><strong>Aims: </strong>A large number of surgical operations are available to treat osteochondral defects of the knee. However, the knee joint arthroplasty materials cannot completely mimic the articular cartilage and subchondral bone, which may bring some obvious side effects. Thus, this study proposed a biocompatible osteochondral repair material prepared from a double-layer scaffold of collagen and nanohydroxyapatite (CHA), consisting of collagen hydrogel as the upper layer of the scaffold, and the composite of CHA as the lower layer of the scaffold.</p><p><strong>Methods: </strong>The CHA scaffold was prepared, and properties including morphology, internal structure, and mechanical strength of the CHA scaffold were measured by scanning electron microscopy (SEM) and a MTS electronic universal testing machine. Then, biocompatibility and repair capability of the CHA scaffold were further evaluated using a rabbit knee cartilage defect model.</p><p><strong>Results: </strong>The CHA scaffold was well suited for the repair of articular cartilage and subchondral bone; the in vitro results showed that the CHA scaffold had good cytocompatibility. In vivo experiments demonstrated that the material had high biocompatibility and effectively induced cartilage and subchondral bone regeneration.</p><p><strong>Conclusion: </strong>The CHA scaffold has a high potential for commercialization and could be used as an effective knee repair material in clinical applications.</p>","PeriodicalId":9074,"journal":{"name":"Bone & Joint Research","volume":"14 2","pages":"155-165"},"PeriodicalIF":4.7,"publicationDate":"2025-02-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11865975/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143514520","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Occurrence of cellular senescence in chronic human shoulder tendinopathies and its attenuation ex vivo by inhibition of Enhancer of Zeste 2.","authors":"Dominik Bühler, Morgane Hilpert, Andrea Barbero, Andreas M Müller, Sebastian A Müller, Ivan Martin, Karoliina Pelttari","doi":"10.1302/2046-3758.142.BJR-2023-0378.R2","DOIUrl":"10.1302/2046-3758.142.BJR-2023-0378.R2","url":null,"abstract":"<p><strong>Aims: </strong>Our aim was to investigate occurrence of senescent cells directly in tendon tissue biopsies from patients with chronic shoulder tendinopathies, and to correlate senescence with Enhancer of zeste 2 (EZH2) expression, the functional subunit of the epigenetic master regulator polycomb repressive complex.</p><p><strong>Methods: </strong>Human proximal long head of biceps tendons from patients with different chronic shoulder pathologies (n = 22), and controls from patients with humerus fracture (n = 6) and pathology (n = 4), were histologically scored for degeneration and analyzed for gene and protein expression of tendon specific factors, senescence markers, and EZH2. Tissues were further exposed to senotherapeutic compounds and the USA Food and Drugs Administration-approved selective EZH2 inhibitor EPZ-6438 and their senescence-associated secretory phenotype (SASP) assessed.</p><p><strong>Results: </strong>Expression of senescence markers (<i>CDKN2A</i>/p16, <i>CDKN2D</i>/p19) and <i>EZH2</i> was significantly higher in tendinopathies compared to fracture or healthy tissue controls and positively correlated with the degree of tissue degeneration. Immunofluorescent stainings demonstrated colocalization of p16 and p19 with EZH2 in tenocytes. Treatment of tendon biopsies with EPZ-6438 reduced secretion of a panel of SASP factors, including interleukin-6 (IL6), IL8, matrix metalloproteinase-3 (MMP3) or GRO1, similarly to the senotherapeutic compound AG490.</p><p><strong>Conclusion: </strong>We demonstrate that senescence traits accumulate in pathological tendon tissues and positively correlate with tissue degeneration. Increased expression of <i>CDKN2A</i>/p16 and <i>CDKN2D</i>/p19 coincides with EZH2 expression, while its inhibition decreased the secretion of SASP factors, indicating a possible regulatory role of EZH2 in tenocyte senescence in tendinopathies. Reduction of cellular senescence, e.g. with EPZ-6438, opens ways to new potential therapeutic approaches for enhancing regeneration in chronic tendinopathies.</p>","PeriodicalId":9074,"journal":{"name":"Bone & Joint Research","volume":"14 2","pages":"143-154"},"PeriodicalIF":4.7,"publicationDate":"2025-02-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11851219/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143490708","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}