Journal of Orthopaedic Translation最新文献

{"title":"The effects and mechanisms of electromagnetic fields on bone remodeling: From clinical to laboratory","authors":"Junyu Liu ,&nbsp;Weihao Ren ,&nbsp;Shenghang Wang ,&nbsp;Jiancheng Yang ,&nbsp;Hao Zhang ,&nbsp;Yuhong Zeng ,&nbsp;Dachuan Yin ,&nbsp;Peng Shang","doi":"10.1016/j.jot.2025.03.003","DOIUrl":"10.1016/j.jot.2025.03.003","url":null,"abstract":"<div><div>Electromagnetic fields (EMFs) are physical fields generated by electrically charged objects, and play a vital role in the growth and development of living organisms. Bone is a highly dynamic structure that undergoes a constant remodeling process. From 1962 to 1977, Bassett discovered the piezoelectric effect in bone tissue and found that EMFs accelerated osteogenesis, promoted tibial fracture healing in dogs, and had positive effects in clinical trials. Since then, EMFs have been increasingly studied in bone remodeling disorders as a non-invasive physical therapy. This review summarizes clinical trials and laboratory studies on EMF interventions in bone remodeling disorders over the past few decades, outlining the effects of EMFs on various bone cells and their underlying molecular mechanisms. In addition, we propose issues in current studies and give an outlook on the research and application of EMFs as a non-invasive physical therapy.</div></div><div><h3>The translational potential of this article</h3><div>This article systematically reviews the research ranging from biological and physical mechanisms to medical applications of EMFs on bone remodeling and related diseases, identifies key challenges in future basic research, and proposes new strategies for developing novel medical equipment and advancing clinical applications in this field. These insights contribute to the advancement of non-invasive physical therapies in orthopedics.</div></div>","PeriodicalId":16636,"journal":{"name":"Journal of Orthopaedic Translation","volume":"52 ","pages":"Pages 14-26"},"PeriodicalIF":5.9,"publicationDate":"2025-03-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143683121","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":"Single-cell transcriptomic analysis reveals AP-1 downregulation remodels bone marrow environment and contributes to osteopenia in ovariectomized mice","authors":"Zhanrong Zhang ,&nbsp;Zhengbo Tao ,&nbsp;Zheng Zhang ,&nbsp;Weijin Zhang ,&nbsp;Xuanrui Zhang ,&nbsp;Xunpei Xu ,&nbsp;Rui Gao ,&nbsp;Xia Tao ,&nbsp;Xuhui Zhou","doi":"10.1016/j.jot.2025.03.001","DOIUrl":"10.1016/j.jot.2025.03.001","url":null,"abstract":"<div><h3>Background</h3><div>Estrogen deficiency-induced osteoporosis largely results from disrupted immune environment in bone marrow, yet the underlying cellular and molecular mechanisms remain incompletely understood. This study aimed to investigate how estrogen deficiency alters bone marrow cellular composition and signaling pathways, with a focus on the regulatory role of activator protein 1 (AP-1) and its impact on osteoclastogenesis.</div></div><div><h3>Methods</h3><div>Single-cell RNA sequencing (scRNA-seq) was performed on bone marrow cells from sham-operated and ovariectomized (OVX) mice to map cell-type-specific changes. AP-1 inhibitor T5224 was administered to validate its functional role in vivo, while in vitro experiments assessed AP-1 activation via estrogen receptor signaling under estrogen stimulation. B lymphogenesis was pharmacologically inhibited using an IL-7 monoclonal antibody in OVX mice to evaluate its therapeutic potential.</div></div><div><h3>Results</h3><div>OVX mice exhibited a marked expansion of proliferative B cells (enriched in protein translation/DNA replication pathways) and reduced neutrophil proportions. scRNA-seq revealed widespread downregulation of AP-1 subunits, namely Fos, Fosb, Jun, Junb, across multiple cell types. T5224-induced AP-1 inhibition recapitulated OVX-associated B cell/neutrophil imbalance and triggered significant bone loss. Mechanistically, estrogen receptor activation upregulated AP-1 under estrogen stimulation, whereas AP-1 inhibition promoted B cell proliferation and increased GM-CSF and RANKL levels, thereby facilitating osteoclastogenesis. Critically, IL-7 antibody-mediated suppression of B lymphogenesis in OVX mice substantially attenuated bone loss.</div></div><div><h3>Conclusion</h3><div>AP-1 downregulation drives estrogen deficiency-related osteopenia by disrupting bone marrow homeostasis, primarily through excessive B cell expansion and elevated osteoclastogenic signaling. Targeting B cell proliferation via IL-7 blockade presents a potential therapeutic strategy for mitigating osteoporosis in estrogen-deficient conditions.</div></div>","PeriodicalId":16636,"journal":{"name":"Journal of Orthopaedic Translation","volume":"52 ","pages":"Pages 1-13"},"PeriodicalIF":5.9,"publicationDate":"2025-03-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143683123","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":"Exploring molecular and cellular signaling pathways: Unraveling the pathogenesis of tendinopathy","authors":"Zihan Xu ,&nbsp;Wenjing Hou ,&nbsp;Tao Zhang ,&nbsp;Rui Chen ,&nbsp;Thomas Skutella","doi":"10.1016/j.jot.2025.02.003","DOIUrl":"10.1016/j.jot.2025.02.003","url":null,"abstract":"<div><div>Despite the long healing duration of tendon injuries, the outcomes of repairs are frequently suboptimal, resulting in persistent pain and reduced functionality. Current clinical approaches to tendinopathy are primarily symptomatic, encompassing nonsteroidal anti-inflammatory drugs (NSAIDs), corticosteroid injections, physical therapies, surgical interventions, loading programs, and pain management. Yet, these treatments have protracted timelines and their efficacy remains uncertain. This uncertainty stems largely from an incomplete understanding of tendinopathy's pathogenesis. Unraveling the mechanisms behind tendinopathy is essential for devising novel therapeutic strategies. In this context, this review systematic reviewed more recent cellular and molecular literature in tendinopathy, in order to summarize the up-to-date advancements including the structure and composition of healthy tendons, the pathophysiological changes in tendinopathy, the molecular pathways implicated in various forms of the condition, and current effective treatment methods. This review not only aims to offer insights but also to inspire further investigation into the mechanisms and clinical management of tendinopathy.</div></div><div><h3>The translational potential of this article</h3><div>A deficient understanding of the molecular mechanisms hampers the advancement of therapeutic strategies and drug development. Consequently, an in-depth examination of these molecular mechanisms is essential for comprehending the etiology of tendinopathy and for devising effective clinical management strategies.</div></div>","PeriodicalId":16636,"journal":{"name":"Journal of Orthopaedic Translation","volume":"51 ","pages":"Pages 298-311"},"PeriodicalIF":5.9,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143682112","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":"ISRIB facilitates post-spinal cord injury recovery through attenuation of neuronal apoptosis and modulation of neuroinflammation","authors":"Qingyang Li ,&nbsp;Chi Zhang ,&nbsp;Enlin Qi ,&nbsp;Mingxin Wu ,&nbsp;Haijian Sun ,&nbsp;Tao Zhang ,&nbsp;Yunpeng Jiang ,&nbsp;Hao Li ,&nbsp;Ruizhi Jiang ,&nbsp;Chuang Li ,&nbsp;Hua Zhao ,&nbsp;Hengxing Zhou ,&nbsp;Shiqing Feng","doi":"10.1016/j.jot.2025.01.003","DOIUrl":"10.1016/j.jot.2025.01.003","url":null,"abstract":"<div><h3>Background</h3><div>Neuronal apoptosis and inflammation are two critical factors that impede functional recovery post spinal cord injury (SCI). Previous studies have demonstrated the inhibitory effects of integrated stress response inhibitor (ISRIB) on neuroinflammation in brain injury. However, whether ISRIB can regulate neuron death and neuroinflammation in the context of SCI remains elusive.</div></div><div><h3>Methods</h3><div>We employed an oxygen-glucose deprivation/reperfusion (OGD/R) model to simulate spinal cord ischemia-reperfusion injury and utilized lipopolysaccharide (LPS) to activate microglia. We assessed cell viability and death to demonstrate the neuroprotective effect of ISRIB against neuron death, while evaluating cytokine levels and the expression of Arg1 and iNOS to elucidate the regulatory role of ISRIB in neuroinflammation. Bulk RNA-seq analysis was employed to investigate the global transcriptional changes in neurons and microglia induced by ISRIB treatment. Additionally, we validated the promoting effects of ISRIB on motor and sensory recovery in a mouse model of SCI.</div></div><div><h3>Results</h3><div>We observed that ISRIB exerted a suppressive effect on neuron death and neuroinflammation. RNA-seq data revealed that the ISRIB exhibited regulation of neuron apoptosis through the P53 signaling pathway, as well as modulation of neuroinflammation by the JAK2/STAT3 signaling pathway. Western blotting and immunofluorescence analyses demonstrated that ISRIB reduced P53 expression in neuronal nuclei and inhibited the phosphorylation of JAK2 and STAT3 in microglia. In addition, we validated the capacity of ISRIB to promote locomotor function recovery in a mouse model of SCI.</div></div><div><h3>Conclusion</h3><div>Our study confirmed the ability of ISRIB to regulate neuron apoptosis and neuroinflammation in SCI via the P53 signaling pathway and the JAK2/STAT3 signaling pathway, respectively. Treatment with ISRIB in mice with SCI promoted the recovery of neural function. This research provides new evidence and options for therapeutic strategies of SCI.</div></div><div><h3>The translational potential of this article</h3><div>Our study provides experimental evidence to support the application of ISRIB in the repair of spinal cord injury.</div></div>","PeriodicalId":16636,"journal":{"name":"Journal of Orthopaedic Translation","volume":"51 ","pages":"Pages 119-131"},"PeriodicalIF":5.9,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143562612","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":"Targeting Piezo1 channel to alleviate intervertebral disc degeneration","authors":"Feiyun Li ,&nbsp;Mingjue Chen ,&nbsp;Mengrui Zhang ,&nbsp;Sheng Chen ,&nbsp;Minghao Qu ,&nbsp;Shuangshuang He ,&nbsp;Lin Wang ,&nbsp;Xiaohao Wu ,&nbsp;Guozhi Xiao","doi":"10.1016/j.jot.2025.01.006","DOIUrl":"10.1016/j.jot.2025.01.006","url":null,"abstract":"<div><h3>Background</h3><div>Low back pain impacts over 600 million people worldwide, predominantly due to intervertebral disc degeneration. This study focuses on the role of Piezo1, a crucial mechanosensitive ion channel protein, in the pathology and potential treatment of disc degeneration.</div></div><div><h3>Materials and methods</h3><div>To investigate the effects of disc-specific Piezo1 deletion, we generated <em>Aggrecan</em>^{<em>CreERT2</em>}<em>; Piezo1</em>^{<em>fl/fl</em>} mice and examined both lumbar spine instability (LSI)- and aging-induced disc degeneration. Additionally, the effect of pharmacological inhibition of Piezo1 was evaluated using GsMTx4, a potent Piezo1 antagonist, in an ex vivo model stimulated with IL-1β to induce disc degeneration. Assessments included histological examinations, immunofluorescence, and western blot analyses to thoroughly characterize the alterations in the intervertebral discs.</div></div><div><h3>Results</h3><div>Elevated expression of Piezo1 was detected in the nucleus pulposus (NP) of intervertebral discs with advanced disc degeneration in both aged mice and human patients. Inducible deletion of Piezo1 expression in aggrecan-expressing disc cells significantly reduced lumbar disc degeneration, decreased extracellular matrix (ECM) degradation, and lowered apoptosis in NP cells, observed in both aged mice and those undergoing LSI surgery. Excessive compression loading (CL) upregulated Piezo1 expression, induced ECM disruption, and increased apoptosis in NP cells, whereas inhibition of Piezo1 with GsMTx4 effectively mitigated these pathological changes. Furthermore, in ex vivo cultured mouse discs, GsMTx4 treatment significantly alleviated IL-1β-induced degenerative damages, restored ECM anabolism, and reduced apoptosis.</div></div><div><h3>Conclusions</h3><div>The findings suggest that Piezo1 plays a critical role in the development of disc degeneration and highlight its potential as a therapeutic target. Inhibiting Piezo1 could offer a novel strategy for treating or preventing this critical disease.</div></div><div><h3>Translational potential of this article</h3><div>This research highlights the involvement of Piezo1 in the development of intervertebral disc degeneration and emphasizes the potential for targeting Piezo1 as a therapeutic strategy to delay or reverse this condition.</div></div>","PeriodicalId":16636,"journal":{"name":"Journal of Orthopaedic Translation","volume":"51 ","pages":"Pages 145-158"},"PeriodicalIF":5.9,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143578971","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 ‘Memantine attenuates the development of osteoarthritis by blocking NMDA receptor mediated calcium overload and chondrocyte senescence’ [2024 Aug 27:48:204-216]","authors":"Qingmei Cheng ,&nbsp;Ke He ,&nbsp;Junyu Zhu ,&nbsp;Xiaoxiao Li ,&nbsp;Xuan Wu ,&nbsp;Chao Zeng ,&nbsp;Guanghua Lei ,&nbsp;Ning Wang ,&nbsp;Hui Li ,&nbsp;Jie Wei","doi":"10.1016/j.jot.2025.02.005","DOIUrl":"10.1016/j.jot.2025.02.005","url":null,"abstract":"","PeriodicalId":16636,"journal":{"name":"Journal of Orthopaedic Translation","volume":"51 ","pages":"Page 176"},"PeriodicalIF":5.9,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143620634","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":"Integration of longitudinal load-bearing tissue MRI radiomics and neural network to predict knee osteoarthritis incidence","authors":"Tianyu Chen ,&nbsp;Jian Chen ,&nbsp;Hao Liu ,&nbsp;Zhengrui Liu ,&nbsp;Bin Yu ,&nbsp;Yang Wang ,&nbsp;Wenbo Zhao ,&nbsp;Yinxiao Peng ,&nbsp;Jun Li ,&nbsp;Yun Yang ,&nbsp;Hang Wan ,&nbsp;Xing Wang ,&nbsp;Zhong Zhang ,&nbsp;Deng Zhao ,&nbsp;Lan Chen ,&nbsp;Lili Chen ,&nbsp;Ruyu Liao ,&nbsp;Shanhong Liu ,&nbsp;Guowei Zeng ,&nbsp;Zhijia Wen ,&nbsp;Yingze Zhang","doi":"10.1016/j.jot.2025.01.007","DOIUrl":"10.1016/j.jot.2025.01.007","url":null,"abstract":"&lt;div&gt;&lt;h3&gt;Background&lt;/h3&gt;&lt;div&gt;Load-bearing structural degradation is crucial in knee osteoarthritis (KOA) progression, yet limited prediction models use load-bearing tissue radiomics for radiographic (structural) KOA incident.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Purpose&lt;/h3&gt;&lt;div&gt;We aim to develop and test a Load-Bearing Tissue plus Clinical variable Radiomic Model (LBTC-RM) to predict radiographic KOA incidents.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Study design&lt;/h3&gt;&lt;div&gt;Risk prediction study.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Methods&lt;/h3&gt;&lt;div&gt;The 700 knees without radiographic KOA at baseline were included from Osteoarthritis Initiative cohort. We selected 2164 knee MRIs during 4-year follow-up. LBTC-RM, which integrated MRI features of meniscus, femur, tibia, femorotibial cartilage, and clinical variables, was developed in total development cohort (n = 1082, 542 cases vs. 540 controls) using neural network algorithm. Final predictive model was tested in total test cohort (n = 1082, 534 cases vs. 548 controls), which integrated data from five visits: baseline (n = 353, 191 cases vs. 162 controls), 3 years prior KOA (n = 46, 19 cases vs. 27 controls), 2 years prior KOA (n = 143, 77 cases vs. 66 controls), 1 year prior KOA (n = 220, 105 cases vs. 115 controls), and at KOA incident (n = 320, 156 cases vs. 164 controls).&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Results&lt;/h3&gt;&lt;div&gt;In total test cohort, LBTC-RM predicted KOA incident with AUC (95 % CI) of 0.85 (0.82–0.87); with LBTC-RM aid, performance of resident physicians for KOA prediction were improved, with specificity, sensitivity, and accuracy increasing from 50 %, 60 %, and 55 %–72 %, 73 %, and 72 %, respectively. The LBTC-RM output indicated an increased KOA risk (OR: 20.6, 95 % CI: 13.8–30.6, p &lt; .001). Radiomic scores of load-bearing tissue raised KOA risk (ORs: 1.02–1.9) from 4-year prior KOA whereas 3-dimensional feature score of medial meniscus decreased the OR (0.99) of KOA incident at KOA confirmed. The 2-dimensional feature score of medial meniscus increased the ORs (1.1–1.2) of KOA symptom score from 2-year prior KOA.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Conclusions&lt;/h3&gt;&lt;div&gt;We provided radiomic features of load-bearing tissue to improved KOA risk level assessment and incident prediction. The model has potential clinical applicability in predicting KOA incidents early, enabling physicians to identify high-risk patients before significant radiographic evidence appears. This can facilitate timely interventions and personalized management strategies, improving patient outcomes.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;The Translational Potential of this Article&lt;/h3&gt;&lt;div&gt;This study presents a novel approach integrating longitudinal MRI-based radiomics and clinical variables to predict knee osteoarthritis (KOA) incidence using machine learning. By leveraging deep learning for auto-segmentation and machine learning for predictive modeling, this research provides a more interpretable and clinically applicable method for early KOA detection. The introduction of a Radiomics Score System enhances ","PeriodicalId":16636,"journal":{"name":"Journal of Orthopaedic Translation","volume":"51 ","pages":"Pages 187-197"},"PeriodicalIF":5.9,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143628459","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":"COPB1 deficiency triggers osteoporosis with elevated iron stores by inducing osteoblast ferroptosis","authors":"Yike Wang ,&nbsp;Ruizhi Zhang ,&nbsp;Aifei Wang ,&nbsp;Xiao Wang ,&nbsp;Xiongyi Wang ,&nbsp;Jiajun Zhang ,&nbsp;Gongwen Liu ,&nbsp;Kai Huang ,&nbsp;Baoshan Liu ,&nbsp;Yutong Hu ,&nbsp;Sheng Pan ,&nbsp;Xieyidai Ruze ,&nbsp;Qiaocheng Zhai ,&nbsp;Youjia Xu","doi":"10.1016/j.jot.2025.01.017","DOIUrl":"10.1016/j.jot.2025.01.017","url":null,"abstract":"<div><h3>Background</h3><div>Osteoporosis (OP) is a systemic bone metabolic disease that results from an imbalance between bone formation and bone resorption. The accumulation of iron has been identified as an independent risk factor for osteoporosis. Ferroptosis, a novel form of programmed cell death, is driven by iron-dependent lipid peroxidation. Nevertheless, the precise role of ferroptosis in iron accumulation-induced osteoporosis remains uncertain.</div></div><div><h3>Methods</h3><div>We utilized proteomics and ELISA to screen key regulatory molecules related to iron accumulation in osteoporosis populations. HE staining was used to assess osteocyte changes in Hamp knockout (KO) iron accumulation mouse models. Western Blot, qPCR, ALP staining, and Alizarin Red staining were employed to explore the effects of siRNA-mediated gene knockdown on osteogenic differentiation in the MC3T3 cell line. ELISA, micro-CT, von Kossa staining, toluidine blue staining, TRAP staining, and calcein analysis were used to study the bone phenotype of conditional gene knockout mice. RNA-seq, endoplasmic reticulum activity probes, transmission electron microscopy (TEM), Western Blot, co-immunoprecipitation (Co-IP), flow cytometry, and ChIP-seq were employed to investigate the regulatory mechanisms of the target gene in osteogenic differentiation. OVX and Hamp KO mice were used to establish osteoporosis models, and AAV-mediated overexpression was employed to explore the intervention effects of the target gene on osteoporosis.</div></div><div><h3>Results</h3><div>The experiments demonstrate that iron accumulation can lead to changes in COPB1 expression levels in bone tissue. Cellular and animal experiments revealed that COPB1 deficiency reduces the osteogenic ability of osteoblasts. Transcriptome analysis and phenotypic experiments revealed that COPB1 deficiency induces ferroptosis and endoplasmic reticulum stress in cells. Further investigation confirmed that COPB1 plays a key role in endoplasmic reticulum stress by inhibits SLC7A11 transcription via ATF6. This reduces cystine uptake, ultimately inducing ferroptosis. Overexpression of COPB1 can restore osteogenic function in both cells and mice.</div></div><div><h3>Conclusion</h3><div>This study elucidated the essential role of COPB1 in maintaining bone homeostasis and highlights it as a potential therapeutic target for treating iron accumulation-related osteoporosis.</div></div><div><h3>The translational potential of this article</h3><div>Our data elucidate the critical role of COPB1 in maintaining bone homeostasis and demonstrate that COPB1 can directly promote bone formation, making it a potential therapeutic target for the future treatment of osteoporosis.</div></div>","PeriodicalId":16636,"journal":{"name":"Journal of Orthopaedic Translation","volume":"51 ","pages":"Pages 312-328"},"PeriodicalIF":5.9,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143682114","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":"Importance to understand medical device regulations for accelerating clinical translation","authors":"Qing Lu ,&nbsp;Yu-Sheng Hsueh ,&nbsp;Wenxue Tong ,&nbsp;Yuantao Zhang ,&nbsp;Jiankun Xu ,&nbsp;Ling Qin","doi":"10.1016/j.jot.2025.02.002","DOIUrl":"10.1016/j.jot.2025.02.002","url":null,"abstract":"<div><div>Clinical translation of medical devices is determined by many factors and is challenging for certain countries or regions as no regulatory body is available to approve related applications. They must rely on application for regulatory bodies of other countries or regions who have independent medical device regulatory systems, while the major markets regulatory process is different. For example, considering the market size and policy orientation, mainland China may be a good option for Hong Kong research organizations. Typically, China National Medical Products Administration (NMPA) has positioned innovation as a key growth engine and implemented various mechanisms to expedite the registration, including Marketing Authorization Holder policy (MAH), as well as the setting up of the NMPA's Guangdong-Hong Kong-Macao Greater Bay Area (GBA) Branch Office, type test reform and application for securing innovation channel application. However, there are still many challenges in the transitional process for Hong Kong universities or research institutions, to set up a company in mainland and then prepare many documental files from very beginning. In the future, taking advantage of NMPA reform and seeking cooperation with the NMPA to establish an independent regulatory body in Hong Kong to be recognized by NMPA is recommended as this alone will boost innovation in life sciences and boost in Hong Kong, and have a positive impact on the commercialization of medical devices in mainland China. Such example may also be relevant for many countries or regions who are seeking medical device approval in the designated regulatory systems.</div></div>","PeriodicalId":16636,"journal":{"name":"Journal of Orthopaedic Translation","volume":"51 ","pages":"Pages 290-297"},"PeriodicalIF":5.9,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143682111","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":"A perspective on reoperations after surgical treatments of degenerative lumbar diseases","authors":"Guoan Li ,&nbsp;Won Man Park ,&nbsp;Thomas Cha","doi":"10.1016/j.jot.2025.01.014","DOIUrl":"10.1016/j.jot.2025.01.014","url":null,"abstract":"<div><div>Clinical data including reoperation rates are comparable for lumbar patients after decompression-alone or decompression-with-fusion surgeries. However, there could exist different mechanisms causing complications after the two surgeries. We discussed research and technology development perspectives for improvement of the surgeries using published clinical outcome data.</div></div>","PeriodicalId":16636,"journal":{"name":"Journal of Orthopaedic Translation","volume":"51 ","pages":"Pages 159-162"},"PeriodicalIF":5.9,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143610180","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}