Journal of Orthopaedic Translation最新文献

{"title":"From cartilage–sensory nerve crosstalk to clinically actionable pain phenotyping in osteoarthritis","authors":"Zhewei Ma, Yiquan Ji","doi":"10.1016/j.jot.2026.101169","DOIUrl":"10.1016/j.jot.2026.101169","url":null,"abstract":"","PeriodicalId":16636,"journal":{"name":"Journal of Orthopaedic Translation","volume":"59 ","pages":"Article 101169"},"PeriodicalIF":9.8,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13355515/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148421851","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Electrical stimulation as an emerging strategy in bone repair: Mechanisms, applications, and advances","authors":"Xue Wang,&nbsp;Huilin Hu,&nbsp;Nana Xiong,&nbsp;Shaoke Gu,&nbsp;Juan Liu","doi":"10.1016/j.jot.2026.101177","DOIUrl":"10.1016/j.jot.2026.101177","url":null,"abstract":"<div><div>The treatment of critical-sized bone defects remains a substantial clinical challenge in orthopaedics. Electrical stimulation (ES), which mimics the endogenous bioelectric and piezoelectric properties of bone tissue, has emerged as a promising non-invasive modality to facilitate bone regeneration. This review elucidates the multifaceted mechanisms through which ES coordinately enhances osteogenesis, angiogenesis, and inflammation resolution, primarily via the regulation of key signalling pathways and modulation of the immune microenvironment at molecular and cellular levels. We also highlight recent advances in the integration of ES with electroactive biomaterials, enabling more targeted and efficacious therapeutic outcomes. Robust clinical evidence supports the ability of ES to significantly accelerate fracture healing, underscoring its translational relevance and potential for broad clinical adoption. By synthesizing these developments, this review aims to inform and inspire the design of next-generation bone regeneration strategies.</div></div><div><h3>The translational potential of this article</h3><div>ES offers a non-invasive or minimally invasive therapeutic modality that can significantly accelerate fracture healing and bone regeneration. This review synthesizes current mechanistic understanding and clinical evidence, highlighting ES as a potential alternative to secondary revision surgery for nonunion fractures. By integrating ES with electroactive biomaterials and emerging self-powered implantable devices, future strategies can be translated into personalized, intelligent bone repair systems, reducing patient morbidity and healthcare costs.</div></div>","PeriodicalId":16636,"journal":{"name":"Journal of Orthopaedic Translation","volume":"59 ","pages":"Article 101177"},"PeriodicalIF":9.8,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13356698/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148430803","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Tendon stem/progenitor cells in heterotopic ossification: functional regulation, molecular mechanisms and targeted therapeutic strategies","authors":"Xuanlin Zhu,&nbsp;Yuan Gao,&nbsp;Minglei Cai,&nbsp;Heng Jiang,&nbsp;Rui Gao,&nbsp;Hao Tang,&nbsp;Tielong Liu,&nbsp;Xuhui Zhou,&nbsp;Bowen Lai","doi":"10.1016/j.jot.2026.101167","DOIUrl":"10.1016/j.jot.2026.101167","url":null,"abstract":"<div><div>Heterotopic ossification (HO) is a pathological process in which ectopic bone tissue forms within soft tissues such as tendons, resulting in pain, limited range of motion, and functional disability that reduces the quality of life. In recent years, tendon stem/progenitor cells (TSPCs) have been considered a key cellular source of HO due to their inherent multilineage differentiation potential. This review aims to systematically elaborate on the advances in the functional regulation and mechanisms of TSPCs in HO. Existing evidence (including lineage tracing and clinical studies) indicates that under the stimulation of trauma, inflammation, and other factors, the chondrogenic and osteogenic differentiation of TSPCs are abnormally activated, shifting their fate from tendon repair to ectopic bone formation. This process is centrally regulated by osteochondrogenesis-related signaling pathways such as BMP, as well as inflammatory signaling pathways such as NF-κB. External factors such as mechanical and inflammatory microenvironment also play important stimulatory roles. Based on these mechanisms, drugs and biomaterials targeting the function of TSPCs have shown potential for the prevention and treatment of HO. Future research needs to explore the heterogeneity of TSPCs and the spatiotemporal dynamics of their regulatory networks, providing theoretical support for the clinical translation of therapeutic strategies.</div></div><div><h3>The translational potential of this article</h3><div>Given the critical role of TSPCs in driving heterotopic ossification through aberrant differentiation, targeting these cells represents a highly promising translational strategy. This review details how external stimuli change the local microenvironment and disrupt the signaling networks within TSPCs, shifting their fate from tissue repair to abnormal bone formation. Highlighting the application of pharmacological agents and biomaterials to precisely modulate the behavior of TSPCs supports a crucial shift toward targeted preventative therapies</div></div>","PeriodicalId":16636,"journal":{"name":"Journal of Orthopaedic Translation","volume":"59 ","pages":"Article 101167"},"PeriodicalIF":9.8,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13355491/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148421895","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"CHIP protects rheumatoid arthritis progression by targeting TRAF6 in arthritis animal models","authors":"Jing Liu,&nbsp;Kaijian Fan,&nbsp;Yilei Yang,&nbsp;Yidan Tang,&nbsp;Song Guo Zheng,&nbsp;Tingyu Wang","doi":"10.1016/j.jot.2026.101175","DOIUrl":"10.1016/j.jot.2026.101175","url":null,"abstract":"<div><h3>Background</h3><div>Carboxyl terminus of HSC70-interacting protein (CHIP) serves as a quality control protein that involves in inflammation and immunity, bone remodeling and tumorigenesis. However, the role of CHIP in joint disease such as rheumatoid arthritis (RA) is less explored.</div></div><div><h3>Methods</h3><div>Wild-type and <em>Chip</em> knockdown mice were used to establish a collagen-induced arthritis (CIA) model to assess arthritis progression through clinical index and histopathological markers (synovial hyperplasia, inflammatory infiltration and cartilage damage). SiRNA and lentivirus were respectively used to knockdown and overexpress CHIP in CIA fibroblast-like synoviocytes (FLS), investigating its regulatory effect on proliferation, migration, invasion and inflammation. Western blotting and immunofluorescence analysis were performed to assess the effect of CHIP on Tumor necrosis factor receptor-associated factor 6 (TRAF6) and to elucidate the underlying mechanism. Adeno-associated virus (AAV) mediated delivery of <em>Chip</em> was used to evaluate its therapeutic effects in CIA mice.</div></div><div><h3>Results</h3><div>CHIP significantly decreased in the synovium of CIA mice and RA patients compare to control. CHIP deficiency exacerbated synovial inflammation, cartilage degradation, and bone erosion in CIA, further underscoring its protective role in joint homeostasis. Moreover, knockdown of CHIP promoted the proliferation, migration and expression of inflammatory cytokines in CIA-FLS, while CHIP overexpression in CIA-FLS showed the opposite results. Mechanistically, CHIP interacted with TRAF6 and promoted the degradation of TRAF6. CHIP inhibited the migration and pro-inflammatory phenotypes of CIA-FLS via TRAF6/p65 pathway. Further, AAV mediated CHIP gene therapy by intra-articular administration effectively attenuated the progression of CIA by inhibiting the synovial inflammation and expression of TRAF6.</div></div><div><h3>Conclusion</h3><div>Collectively, these findings demonstrated the critical regulatory role of CHIP in RA. Therefore, exploiting the protective effects of CHIP may represent a potential therapeutic strategy for RA.</div></div><div><h3>The translational potential of this article</h3><div>These findings not only advance our understanding of CHIP's regulatory role in RA but also highlight the value of genetic animal models in orthopaedic drug discovery.</div></div>","PeriodicalId":16636,"journal":{"name":"Journal of Orthopaedic Translation","volume":"59 ","pages":"Article 101175"},"PeriodicalIF":9.8,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148554089","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Retraction notice to “Regulating inflammation microenvironment and tenogenic differentiation as sequential therapy promotes tendon healing in diabetic rats” [J Orthop Transl 53(2025) 63-81]","authors":"Jingyi Dang,&nbsp;Zhao Zhang,&nbsp;Jun Fu,&nbsp;Liguo Sun,&nbsp;Yubo Shi,&nbsp;Lei Wang,&nbsp;Weidong Tao,&nbsp;Debin Cheng,&nbsp;Xiaohe Wang,&nbsp;Zhenzhou Mi,&nbsp;Dong Liu,&nbsp;Hongbin Fan","doi":"10.1016/j.jot.2026.101183","DOIUrl":"10.1016/j.jot.2026.101183","url":null,"abstract":"","PeriodicalId":16636,"journal":{"name":"Journal of Orthopaedic Translation","volume":"59 ","pages":"Article 101183"},"PeriodicalIF":9.8,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148634123","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Long-term evaluation of plasma electrolytic oxidation (PEO) surface-modified WE43MEO magnesium alloy screws and plates reveals safe and controlled degradation in a 18-month minipig model","authors":"Alexander Kopp,&nbsp;Alina Schmitz,&nbsp;Henri Kreiker,&nbsp;Heilwig Fischer,&nbsp;Ana Prates Soares,&nbsp;Katharina Schmidt-Bleek,&nbsp;Georg Duda,&nbsp;Henning Hanken,&nbsp;Nadja Kröger,&nbsp;Max Heiland,&nbsp;Ralf Smeets,&nbsp;Carsten Rendenbach","doi":"10.1016/j.jot.2026.101132","DOIUrl":"10.1016/j.jot.2026.101132","url":null,"abstract":"<div><h3>Background</h3><div>Magnesium-based implants are increasingly investigated as bioabsorbable materials for temporary osteosynthesis applications due to their favorable biocompatibility and bone-like elastic modulus. However, controlling the degradation rate remains a critical barrier to clinical translation, as rapid corrosion can compromise mechanical integrity and lead to adverse effects, such as gas formation.</div></div><div><h3>Methods</h3><div>PEO-modified WE43MEO (WE43-PEO) and non-modified WE43MEO screws and plates were implanted in the humerus and femur of Göttinger minipigs in a non-fracture model and assessed after 18 months. Explants were analyzed using micro-computed tomography and non-decalcified histology with histomorphometric quantification of residual implant structure and peri-implant bone response.</div></div><div><h3>Results</h3><div>No significant differences in cortical implant volume were observed. However, PEO modified implants were surrounded by significantly higher volumes of lamellar bone, suggesting reduced remodeling and improved bone integration. Non-modified WE43MEO implants underwent complete degradation, while PEO modified implants showed partial resorption with preserved structure, indicating effective degradation control. Both implant types remained integrated without long-term complications.</div></div><div><h3>Conclusion</h3><div>PEO surface modification of WE43 magnesium implants supports predictable, biocompatible long-term degradation and promotes favorable bone quality without late complications, underscoring the potential of surface-engineered magnesium fixation devices for load-bearing applications.</div></div><div><h3>The translational potential of this article</h3><div>PEO-modified WE43MEO osteosynthesis systems may offer clinically relevant, bioabsorbable fixation with controlled degradation and improved long-term bone integration, potentially reducing implant-related complications and the need for secondary removal procedures in orthopaedic and craniomaxillofacial surgery.</div></div>","PeriodicalId":16636,"journal":{"name":"Journal of Orthopaedic Translation","volume":"59 ","pages":"Article 101132"},"PeriodicalIF":9.8,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13320413/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148368777","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Neurogenic heterotopic ossification: from molecular mechanisms to clinical treatment","authors":"Zhengqiang Yuan,&nbsp;Linbin Xu,&nbsp;Juehong Li,&nbsp;Cunyi Fan","doi":"10.1016/j.jot.2026.101176","DOIUrl":"10.1016/j.jot.2026.101176","url":null,"abstract":"<div><div>Neurogenic heterotopic ossification (NHO), a disabling complication of severe central nervous system injuries, involves ectopic periarticular bone formation that causes profound functional impairments and reduced quality of life. This review highlights recent advances in NHO, especially focusing on the neuro-immune-osteogenic axis. Rather than a merely local disorder, NHO is a systemic response driven by neural, inflammatory, and interorgan signals, notably involving BMP/Smad, macrophage activation, and neuropeptide pathways. While combined-injury animal models advance mechanistic insights, they incompletely replicate human disease heterogeneity. Clinically, early diagnosis is hindered by nonspecific symptoms and insensitive radiography. Current treatments are mainly preventive or symptomatic, lacking efficacy for mature lesions. We highlight that addressing controversies in prophylaxis, surgical timing, and biomarker utility is essential. Future progress relies on validated early biomarkers, standardized imaging, mechanism-based therapeutics, and multidisciplinary precision management.</div><div>The Translational Potential of this Article.</div><div>This review highlights clinical mechanisms and emerging targets for NHO, which may enable earlier diagnosis, individualized prevention, and targeted treatment for patients with central nervous system injury.</div></div>","PeriodicalId":16636,"journal":{"name":"Journal of Orthopaedic Translation","volume":"59 ","pages":"Article 101176"},"PeriodicalIF":9.8,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13380059/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148497785","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Corrigendum to ‘Author's reply to the letter regarding “CMTM6 promotes synovial proliferation and macrophage polarization by preventing ubiquitination of TAK1 in rheumatoid arthritis”’ [J Orthop Transl 2026 Mar 26;57:101087]","authors":"Xiaomeng Luo,&nbsp;Lingling Xu,&nbsp;Juan Cai,&nbsp;Siyang Ma,&nbsp;Haining Song,&nbsp;Pingting Yang,&nbsp;Chunshu Yang","doi":"10.1016/j.jot.2026.101152","DOIUrl":"10.1016/j.jot.2026.101152","url":null,"abstract":"","PeriodicalId":16636,"journal":{"name":"Journal of Orthopaedic Translation","volume":"59 ","pages":"Article 101152"},"PeriodicalIF":9.8,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13316153/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148361160","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hypoxia-preconditioned mitochondrial transplantation multidirectionally modulates Schwann cell functions to repair peripheral nerve injury in rats","authors":"Jin Dong,&nbsp;Bing Yan,&nbsp;Xushen Zhao,&nbsp;Jinyu Bai,&nbsp;Huajian Shan,&nbsp;Xiang Gao,&nbsp;Lei Sheng,&nbsp;Jun Dai,&nbsp;Fengxian Jiang,&nbsp;Mingchao Zhang,&nbsp;Chaowen Bai,&nbsp;Xiaozhong Zhou,&nbsp;Shuai Wei","doi":"10.1016/j.jot.2026.101171","DOIUrl":"10.1016/j.jot.2026.101171","url":null,"abstract":"<div><h3>Background</h3><div>Peripheral nerve injury (PNI) often leads to sensory and motor dysfunction. This study investigated the promoting effect of hypoxia-preconditioned mitochondrial transplantation on the structural and functional reconstruction of peripheral nerves and the molecular mechanisms involved.</div></div><div><h3>Methods</h3><div>We explored the effects of hypoxia-preconditioned mitochondrial transplantation on Schwann cell (SC) phenotypes, including proliferation, migration, cellular senescence, and mitochondrial membrane potential, and explored the underlying molecular mechanism through Western blotting. We assessed axonal and myelin regeneration, as well as motor function recovery, in injured rats through behavioral tests, morphological analysis, and electrophysiological detection.</div></div><div><h3>Results</h3><div>Hypoxia preconditioning significantly increased the mitochondrial membrane potential in SCs without altering their ultrastructure or the normal expression of the COX IV and TOMM20 proteins. The uptake efficiency of SCs for exogenous mitochondria was significantly greater than that of neurons, endothelial cells, fibroblasts, and other cells. Hypoxia-preconditioned mitochondrial transplantation activated the MAPK (Ras-ERK-c-Fos/c-Jun) pathway; promoted SC proliferation, migration, and dedifferentiation; inhibited H₂O₂-induced cellular senescence; and partially restored the mitochondrial membrane potential. Hypoxia-preconditioned mitochondrial transplantation significantly accelerated axonal growth, promoted axonal remyelination, led to significant recovery of electrophysiological function, and improved motor function.</div></div><div><h3>Conclusion</h3><div>Hypoxia preconditioning enhances the mitochondrial membrane potential of SC-derived mitochondria. Mitochondrial transplantation modulates SC functions by activating the Ras-ERK-c-Fos/c-Jun pathway, significantly increases nerve fiber density and myelin thickness, alleviates gastrocnemius muscle atrophy, and promotes motor function recovery, providing a new strategy for the clinical treatment of PNI.</div></div><div><h3>Translational potential</h3><div>We established a hypoxia-preconditioned mitochondrial transplantation method that modulates SC functions, accelerates axonal and myelin regeneration, and promotes motor function recovery. This study provides a novel clinical strategy for treating peripheral nervous system injuries.</div></div>","PeriodicalId":16636,"journal":{"name":"Journal of Orthopaedic Translation","volume":"59 ","pages":"Article 101171"},"PeriodicalIF":9.8,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148554088","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Self-assembled meniscus-specific ECM membrane promotes cell migration and vascular ingrowth for meniscus repair and reconstruction","authors":"Mingze Du,&nbsp;Yuwei Wang,&nbsp;Tuo Wu,&nbsp;Huinan Lai,&nbsp;Liya Ai,&nbsp;Jiajun Liu,&nbsp;Ting Zhu,&nbsp;Jingke Du,&nbsp;Jun Yin,&nbsp;Dong Jiang","doi":"10.1016/j.jot.2026.101141","DOIUrl":"10.1016/j.jot.2026.101141","url":null,"abstract":"&lt;div&gt;&lt;h3&gt;Background&lt;/h3&gt;&lt;div&gt;The knee meniscus has limited intrinsic repair and regenerative capacity. Safe and effective biotherapeutic products remain lacking, and enhancing cell migration and angiogenesis remains a major challenge. This study aimed to develop a novel self-assembled meniscus-specific extracellular matrix membrane (saECM-M) and evaluate its performance in scaffold-free meniscus repair and scaffold-guided whole-meniscus reconstruction, in comparison with chemically processed decellularized ECM (cpd-ECM).&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Methods&lt;/h3&gt;&lt;div&gt;Meniscal fibrochondrocytes (MFCs) were cultured under membrane-inducing conditions to generate saECM-M &lt;em&gt;in vitro&lt;/em&gt;. Its bioactivity was evaluated by cell migration and endothelial network formation assays &lt;em&gt;in vitro&lt;/em&gt; and by a scaffold-free meniscus defect repair model &lt;em&gt;in vivo&lt;/em&gt;. For whole-meniscus reconstruction, saECM-M was integrated with a biomimetic 3D-printed poly(ε-caprolactone) (PCL) scaffold to guide ECM alignment and provide mechanical support. PCL scaffolds seeded with MFCs alone or combined with cpd-ECM served as controls. Meniscus regeneration was assessed in a rabbit meniscectomy model using imaging, histological, and biomechanical analyses, including chondroprotective evaluation. Transcriptomic profiling and proteomics were performed to investigate molecular pathways associated with saECM-M-mediated cell migration and vascular ingrowth.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Results&lt;/h3&gt;&lt;div&gt;saECM-M was characterized as a cell-laden membrane enriched with native meniscus-like ECM components. &lt;em&gt;In vitro&lt;/em&gt;, saECM-M significantly enhanced cell migration and endothelial network formation compared with cpd-ECM (approximately 1.2-fold and 2-fold, respectively; &lt;em&gt;P&lt;/em&gt; &lt; 0.05), accompanied by increased collagen deposition. &lt;em&gt;In vivo&lt;/em&gt;, isolated saECM-M promoted superior meniscus defect repair. When integrated with the biomimetic PCL scaffold, saECM-M further promoted aligned collagen organization, vascular ingrowth, and robust meniscus regeneration. Compared with the PCL-cpd-ECM group, the PCL-saECM-M group showed improved host tissue integration on MRI (WORMS score: 10 ± 1 vs 32.3 ± 2.1), enhanced tensile mechanical properties (79 ± 2 MPa vs 64 ± 7.8 MPa), and superior chondroprotective effects (Mankin score: 1.67 ± 0.58 vs 6.67 ± 0.58) (&lt;em&gt;P&lt;/em&gt; &lt; 0.05). Transcriptomic and proteomic analyses identified enrichment of ECM-receptor interaction- and PI3K-AKT signaling-related pathways associated with saECM-M-enhanced cell migration and vascular ingrowth.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Conclusion&lt;/h3&gt;&lt;div&gt;saECM-M functions as an intrinsically bioactive meniscus-derived matrix capable of promoting both scaffold-free repair and scaffold-guided reconstruction. Compared with cpd-ECM, saECM-M more effectively supports cell migration, angiogenesis, and organized collagen remodeling, leading to superior regenerative outcomes.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;The translational potential of this artic","PeriodicalId":16636,"journal":{"name":"Journal of Orthopaedic Translation","volume":"59 ","pages":"Article 101141"},"PeriodicalIF":9.8,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148554090","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}