Connective Tissue Research最新文献

{"title":"5α-dihydrotestosterone upregulates interferon signaling and limits osteoclast differentiation during inflammatory state.","authors":"Kiana Chen, Michael Christof, Gulzada Kulzhanova, Chia-Lung Wu, Homaira Rahimi","doi":"10.1080/03008207.2026.2642775","DOIUrl":"10.1080/03008207.2026.2642775","url":null,"abstract":"<p><strong>Purpose: </strong>Rheumatoid arthritis is characterized by inflammatory erosions and increased prevalence in females. Androgen, the dominant sex hormone in males, is protective against bone loss. Here, we investigated the cellular targets of androgen and hypothesized that androgen negatively regulates TNFα-driven osteoclastogenesis.</p><p><strong>Materials and methods: </strong>Bone marrow-derived cells from a C57BL/6J mouse femur and tibia were plated with 10^-9M of 5α-dihydrotestosterone (DHT) or vehicle then collected for flow cytometry and flow sorting. Osteoclast precursors (OCPs), myeloid-like CD11b+Gr-1- cells, were grown to osteoclasts then fixed and TRAP-stained. Osteoclasts were quantified by cell counting. Single-cell RNA-sequencing was performed on DHT or vehicle-treated TNFα-stimulated cells, and the differences in cell populations, gene expression, gene ontology, and cell trajectory were analyzed via bioinformatic approaches. RT-qPCR validated sequencing results.</p><p><strong>Results: </strong>DHT-treated OCPs were decreased versus vehicle-treated OCPs (Vehicle = 12.43 ± 0.53%, DHT = 9.93 ± 0.85%, <i>p</i> < 0.05), and there was decreased differentiation from OCPs to osteoclasts (Vehicle = 403.3 ± 141.5, DHT = 10.67 ± 14.36, <i>p</i> < 0.01). Analysis identified osteoclastogenesis-related clusters that varied between samples and interferon-related processes upregulated with DHT treatment. Analysis also determined that DHT treatment may be associated with expression of the transcription factor Irf7. Isg15, the most differentially expressed gene in the DHT-treated clusters, may also be involved in osteoclastogenesis.</p><p><strong>Conclusions: </strong>In summary, androgen targets OCPs and limits their differentiation into osteoclasts. In myeloid populations, DHT treatment results in differential expression of interferon-related processes and genes and alters the trajectory of cells, potentially regulating osteoclastogenesis.</p>","PeriodicalId":10661,"journal":{"name":"Connective Tissue Research","volume":" ","pages":"258-272"},"PeriodicalIF":1.9,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147467188","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":"E3 ubiquitin ligase Peli3 regulates M2 macrophage-to-myofibroblast transition and fibrosis in wound healing via IRF4.","authors":"Jinglin Zhu, Fangning Zhao, Gao Zeng","doi":"10.1080/03008207.2026.2658059","DOIUrl":"10.1080/03008207.2026.2658059","url":null,"abstract":"<p><strong>Purpose: </strong>M2 macrophage-to-myofibroblast transformation (MMT) contributes to fibrosis. The role of interferon regulatory factor 4 (IRF4), a key transcription factor in M2 macrophage polarization, in M2 MMT remains unclear. This study aimed to elucidate the role of IRF4 in M2 MMT.</p><p><strong>Materials and methods: </strong>An in vitro M2 MMT model was established using RAW264.7 macrophages stimulated with transforming growth factor-β1. Cellular phenotypic shift and extracellular matrix (ECM)-associated proteins were detected. The regulatory role of Peli3 in IRF4 ubiquitination modification was assessed. In a full-thickness skin defect mouse model, the regulatory effects of PELI3 on scar fibrosis and the MMT process were evaluated through AAV-mediated overexpression of PELI3.</p><p><strong>Results: </strong>In M2 MMT, IRF4 protein levels were significantly upregulated while ubiquitination levels decreased. Knockdown of IRF4 inhibited M2 polarization and M2 MMT and reduced expression of ECM-associated proteins. Peli3 was significantly downregulated in M2 MMT, and its overexpression suppressed IRF4 protein levels, disrupting M2 MMT and ECM deposition. To directly validate the role of IRF4 in M2 MMT, functional rescue experiments were conducted in PELI3-overexpressing cells. The results demonstrated that overexpressing IRF4 partially reversed the MMT inhibition induced by PELI3 overexpression. Peli3 accelerated IRF4 degradation by promoting its ubiquitin modification. In vivo, Peli3 overexpression reduced fibrosis and MMT.</p><p><strong>Conclusions: </strong>IRF4 promotes M2 MMT and fibrosis progression, with its stability regulated by Peli3-mediated ubiquitination.</p>","PeriodicalId":10661,"journal":{"name":"Connective Tissue Research","volume":" ","pages":"308-320"},"PeriodicalIF":1.9,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147764853","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":"Lumican stimulates osteogenic differentiation in bone marrow-derived mesenchymal stem cells through glycolytic reprogramming to alleviate osteoporosis.","authors":"Heqing Huang, Lei Xiang, Wei Liu, Congcong Zeng, Zhitao Liu","doi":"10.1080/03008207.2025.2596769","DOIUrl":"10.1080/03008207.2025.2596769","url":null,"abstract":"<p><strong>Purpose: </strong>Lumican, a small leucine-rich proteoglycan, is implicated in diverse biological functions. This study investigates the role of lumican in osteogenic differentiation of human bone marrow-derived mesenchymal stem cells (hBMSCs) and its therapeutic efficacy against osteoporosis (OP), while preliminarily elucidating its mechanism.</p><p><strong>Materials and methods: </strong>hBMSCs were cultured under osteogenic induction. Cell proliferation and migration were assessed using CCK-8 and Transwell assays. Osteogenic differentiation was evaluated by ALP/ARS staining, with osteogenic marker genes (Runx2, Osterix, OCN) measured via RT-qPCR. An ovariectomized (OVX) rat OP model was established. Bone microstructure was analyzed by HE staining and serum OCN levels by ELISA. Glycolysis was assessed through glucose uptake, lactate production, ATP levels, and key glycolytic enzyme expression. The glycolytic inhibitor 2-DG was used for rescue experiments. Histone lactylation (H3K18la) and its promoter enrichment were analyzed by Western blot and ChIP.</p><p><strong>Results: </strong>Lumican expression increased during osteogenic induction and dose-dependently enhanced hBMSC proliferation, migration, and osteogenic differentiation. ALP/ARS staining showed. Enhanced osteogenic differentiation, while RT-qPCR further confirmed upregulated Runx2, Osterix, and OCN. In OVX rats, lumican improved trabecular microstructure and increased serum OCN and osteogenic gene expression in bone tissues. Mechanistically, lumican promoted glycolysis in hBMSCs, indicated by increased glucose uptake, lactate production, ATP levels, and glycolytic enzyme expression. The lumican-induced osteogenic effects were abolished by 2-DG. Furthermore, lumican enhanced histone lactylation, particularly increasing H3K18la enrichment at osteogenic gene promoters, which was suppressed by 2-DG.</p><p><strong>Conclusions: </strong>Lumican promotes hBMSC osteogenic differentiation and ameliorates OP by enhancing glycolysis and histone lactylation, providing a potential therapeutic target.</p>","PeriodicalId":10661,"journal":{"name":"Connective Tissue Research","volume":" ","pages":"185-196"},"PeriodicalIF":2.1,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145654029","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":"Nutrient deprivation of tendon-derived cells and its effect on collagen matrix integrity - mimicking graft remodelling after ACL reconstruction <i>in vitro</i> running title: cell starvation vs collagen integrity.","authors":"Amal K Mansoor, Sylvia Dekker, Keita Ito, Jasper Foolen","doi":"10.1080/03008207.2026.2624820","DOIUrl":"10.1080/03008207.2026.2624820","url":null,"abstract":"<p><strong>Purpose: </strong>After anterior cruciate ligament reconstruction surgeries, tendon grafts lose their mechanical integrity in vivo. Both auto- and allografts contain dead cells, and remaining viable cells are restricted temporarily from abundant nutrient access. To evaluate a possible connection, nutrient deprivation was hypothesized to reduce cell viability, compromising tissue mechanics as cells adopt a catabolic state.</p><p><strong>Materials and methods: </strong>Taking inspiration from the graft environment, collagenous tendon-mimics with tendon-derived cells were reconstituted <i>in vitro</i>. Subsequently, tendon-mimics were cultured at varying glucose and serum concentrations, ranging from complete medium (5 mM glucose, 2.5% serum), to mild deprivation (0.5 mM glucose, no serum), extreme deprivation (0 mM glucose, no serum), and a frozen control group (0 mM glucose, no serum).</p><p><strong>Results: </strong>In the complete medium group, cell viability remained stable, improving tendon-mimic mechanics. Tendon cells were resilient to mild nutrient deprivation, maintaining viability. However, at extreme nutrient deprivation or tissue freezing, cell viability dropped significantly. Surprisingly, mechanical properties remained unaltered in all the groups, except the complete medium group. MMP8 secretion and activation confirmed a catabolic potential only in the complete medium group, while no further MMPs were secreted or activated in the nutrient-deprived groups. This suggests that viable cells that are exposed to a nutrient deprived environment likely lack the energy to exert contractile forces or produce/activate MMPs.</p><p><strong>Conclusions: </strong>This study revealed that tendon-derived cells do not compromise collagenous tendon-mimic integrity under nutrient-deprived conditions in an <i>in vitro</i> model, highlighting the resilience of tenocytes in maintaining tissue structure.</p>","PeriodicalId":10661,"journal":{"name":"Connective Tissue Research","volume":" ","pages":"197-209"},"PeriodicalIF":1.9,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146177958","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":"Achilles tendons of MRL/MpJ mice show scar-mediated healing after tenotomy.","authors":"Ningfeng Tang, Divya S Sivalingam, Kimberly Wilson, Mehari M Weldemariam, Hongying Tian, Christoph D Hart, Prishasai Ramnath, Jacob Glazier, Jie Jiang, Natalie Leong, Tao Lowe, Maureen A Kane, Masahiro Iwamoto, Catherine K Kuo, Motomi Enomoto-Iwamoto","doi":"10.1080/03008207.2025.2594694","DOIUrl":"10.1080/03008207.2025.2594694","url":null,"abstract":"<p><strong>Purpose/aim of the study: </strong>Tendon healing in Murphy Roths Large (MRL/MpJ) mice was examined using an Achilles tendon tenotomy model, a full transection model, to compare with previous studies in which regenerative tendon healing was shown in a patellar tendon focal injury model.</p><p><strong>Materials and methods: </strong>Achilles tendons of MRL/MpJ and C57BL/6J mice were fully transected. Tensile testing and proteomics analysis were performed after four weeks of healing. MicroCT was performed after 10 weeks of healing.</p><p><strong>Results: </strong>The Achilles tendons of MRL/MpJ mice healed via scar formation, regardless of sex, as did C57BL/6J mice. Tensile testing found that mechanical properties of injured tendons of both MRL/MpJ female and male mice were similar to those of C57BL/6J female and male mice, respectively, after four weeks of healing, which is during the remodeling phase. After 10 weeks of healing, injured tendons of MRL/MpJ mice possessed smaller heterotopic ossification volumes than those of C57BL/6J mice. Proteomics analysis revealed similar alterations to signaling pathways in injured tendons of MRL/MpJ and C57BL/6J male mice after four weeks of healing. However, among the altered pathways, actin cytoskeleton and integrin signaling pathways were two of the top pathways that were more prominently activated in C57BL/6J males than in MRL/MpJ males.</p><p><strong>Conclusions: </strong>These findings indicate that MRL/MpJ mice possess limited capacity to regenerate injured tendons after complete rupture, and that tenotomized Achilles tendons of MRL/MpJ male mice have lesser induction of heterotopic ossification and lower activation of the signaling pathways also induced with injury in C57BL/6J male mice.</p>","PeriodicalId":10661,"journal":{"name":"Connective Tissue Research","volume":" ","pages":"174-184"},"PeriodicalIF":1.9,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145699988","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":"Mettl3-modified lncRNA Snhg16 aggravates osteoarthritis via promoting chondrocyte ferroptosis by regulating Snd1/Gpx4 axis.","authors":"Qiang Li, Xiangyang Ye, Xiao Yuan, Shengtao Chen, Haibin Tang, Liming Shen, Shangwen He","doi":"10.1080/03008207.2026.2627517","DOIUrl":"10.1080/03008207.2026.2627517","url":null,"abstract":"<p><strong>Purpose/aim: </strong>Long noncoding RNA (lncRNA) small nucleolar RNA host gene 16 (Snhg16) has been confirmed to accelerate osteoarthritis (OA) progress. However, its regulatory mechanism has not been fully elucidated.</p><p><strong>Materials and methods: </strong>Interleukin-1β (IL-1β)-induced ATDC5 chondrocytes were used to mimic OA cell models, and destabilization of medial meniscus (DMM) surgery was performed to construct OA mice models. The expression levels of Snhg16, glutathione peroxidase 4 (Gpx4), staphylococcal nuclease domain-containing 1 (Snd1), methyltransferase-like 3 (Mettl3) and extracellular matrix (ECM) degradation-related markers were detected by qRT-PCR or western blot. Besides, glutathione (GSH), malondialdehyde (MDA), Fe²⁺ and lipid reactive oxygen species (ROS) levels were detected to evaluate cell ferroptosis. The interaction between Snd1 and Snhg16 or Gpx4 was evaluated by RNA pull-down and RNA immunoprecipitation (RIP) assays. The stability of Gpx4 mRNA and Snhg16 was examined using actinomycin D assay. Methylated RNA immunoprecipitation (MeRIP) assay was used to measure the regulation of Mettl3 on Snhg16.</p><p><strong>Results: </strong>Snhg16 downregulation repressed IL-1β-induced chondrocyte ferroptosis and ECM degradation. Also, silencing of Snhg16 alleviated cartilage tissue damage in OA mice models. In the terms of mechanism, Snhg16 inhibited the stability of Gpx4 mRNA via interacting with Snd1. Moreover, Mettl3 enhanced Snhg16 stability by m6A modification. Functional experiments showed that Mettl3 knockdown suppressed IL-1β-induced ferroptosis and ECM degradation through regulating the Snhg16/Snd1/Gpx4 axis.</p><p><strong>Conclusions: </strong>Mettl3-mediated m6A modification of Snhg16 facilitated ferroptosis and ECM degradation to aggravate OA process via regulating Snd1/Gpx4 axis, providing a novel target for OA treatment.</p>","PeriodicalId":10661,"journal":{"name":"Connective Tissue Research","volume":" ","pages":"210-221"},"PeriodicalIF":1.9,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146200391","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":"Flow cytometric identification of dynamic immune cell populations in a rat model of post-traumatic elbow contracture.","authors":"Rebecca F Reals, J Caleb Snider, Ryan M Castile, Chelsey L Dunham, Necat Havlioglu, Paul C Cannon, Benjamin M Zmistowski, Aaron M Chamberlain, Matthew R Bersi, Spencer P Lake","doi":"10.1080/03008207.2025.2593877","DOIUrl":"10.1080/03008207.2025.2593877","url":null,"abstract":"<p><strong>Purpose/aim: </strong>Post-traumatic joint contracture (PTJC) commonly occurs after elbow injury. Previous findings implied immune system activation in capsules of contracted joints; however, quantifying immune cell populations in rodent joint tissues is challenging due to small size and low cellularity. Here, we used flow cytometry to investigate the temporal immune response and enumerate cell populations in the rat elbow capsule after traumatic injury.</p><p><strong>Materials and methods: </strong>After inducing PTJC, capsules were harvested from injured, sham, and control rat elbows at multiple time points, stained with surface markers for immune cells, and quantified via flow cytometry. Results were compared to previously published mechanics and histology data from the same model. Another injured group was treated with celecoxib to determine if changes due to anti-inflammatory treatment could be detected.</p><p><strong>Results: </strong>Compared to control, injured animals displayed elevated leukocytes, T cells, and natural killer cells. CD45+ cells exhibited similar temporal changes as mechanics, which increased and then decreased after injury. CD3+, CD4+, and CD8a+ T cells followed a similar pattern as histology scores, which increased and remained elevated. Treating injured animals with celecoxib increased leukocytes but decreased several immune subpopulations.</p><p><strong>Conclusions: </strong>A method for flow cytometry on rat elbow capsule was established and used to quantify immune cell populations, which changed in response to injury and anti-inflammatory treatment. Comparisons between flow cytometry and previously published mechanics and histology revealed additional insights about temporal patterns in cell-, tissue-, and joint-level changes. Future work will investigate whether changes in immune cells attenuate PTJC symptoms.</p>","PeriodicalId":10661,"journal":{"name":"Connective Tissue Research","volume":" ","pages":"157-173"},"PeriodicalIF":1.9,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13233149/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145667524","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The nuclear localization sequence and C-terminus of parathyroid hormone-related protein regulate chondrocyte development in epiphyseal growth cartilage.","authors":"Waleed J Hashmi, Nathan K Hoggard, Noriko Kantake, Ibiagbani M Max-Harry, Jeremy Kane, Shouan Zhu, Blake E Hildreth, Ramiro E Toribio, Rachelle W Johnson, Thomas J Rosol","doi":"10.1080/03008207.2025.2571548","DOIUrl":"10.1080/03008207.2025.2571548","url":null,"abstract":"<p><strong>Purpose/aim: </strong>Parathyroid hormone -related protein (PTHrP) regulates skeletal development by controlling epiphyseal growth cartilage. In mice, PTHrP contains three functional domains: the N-terminus, nuclear localization sequence (NLS), and C-terminus. The PTHrP (67 -139) region contains both the NLS and the C-terminus. Our research group previously generated C57BL/6 mice lacking this region (<i>Pthrp</i> Δ/Δ), resulting in reduced postnatal growth and shorter stature. This study aimed to define the functional role of PTHrP (67 -139) in chondrocytes in vitro and ex vivo.</p><p><strong>Materials and methods: </strong>Epiphyseal growth cartilage from 1 -2-day-old Pthrp Δ/Δ mice was evaluated using histology, immunofluorescence, and qPCR. Primary chondrocytes from Pthrp Δ/Δ mice and PTHrP-transfected chondrocytes were cultured to assess proliferation and gene expression.</p><p><strong>Results: </strong><i>Pthrp</i> Δ/Δ mice showed significantly reduced epiphyseal cartilage height, including decreased resting, proliferative, and hypertrophic zone lengths. This was accompanied by increased mRNA expression of hypertrophic markers (<i>Ihh, Col10a1</i>). Epiphyseal cartilage from <i>Pthrp</i> Δ/Δ mice also exhibited elevated <i>Adamts5</i> and <i>Mmp13</i> expression, indicating enhanced extracellular matrix degradation. Primary chondrocytes from <i>Pthrp</i> Δ/Δ mice and chondrocytes transiently transfected with the PTHrP deletion construct (ΔNLS+CTERM) showed reduced proliferation and matrix production. Chondrocytes lacking PTHrP (67 -139) had decreased expression of <i>Col2a1</i> and <i>Acan</i>, along with reduced IGF-1/IGF-1R expression, suggesting impaired IGF-1 signaling.</p><p><strong>Conclusions: </strong>Loss of the PTHrP (67 -139) domain causes impaired proliferation, reduced matrix production, and increased extracellular matrix degradation in epiphyseal chondrocytes. These findings demonstrate that PTHrP (67 -139) is required to maintain chondrocytes in an immature state and that its absence leads to premature differentiation of epiphyseal growth plate chondrocytes.</p>","PeriodicalId":10661,"journal":{"name":"Connective Tissue Research","volume":" ","pages":"125-139"},"PeriodicalIF":2.1,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145573358","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":"Correction.","authors":"","doi":"10.1080/03008207.2025.2586413","DOIUrl":"10.1080/03008207.2025.2586413","url":null,"abstract":"","PeriodicalId":10661,"journal":{"name":"Connective Tissue Research","volume":" ","pages":"223"},"PeriodicalIF":2.1,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145494934","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":"Statement of Removal: Microengineering the synovial membrane microenvironment for osteoarthritis research.","authors":"","doi":"10.1080/03008207.2025.2534723","DOIUrl":"10.1080/03008207.2025.2534723","url":null,"abstract":"","PeriodicalId":10661,"journal":{"name":"Connective Tissue Research","volume":" ","pages":"222"},"PeriodicalIF":2.1,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144741380","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}