Bone Research最新文献

{"title":"Biomolecular condensates as dynamic regulators of musculoskeletal homeostasis, disease, and therapeutic challenges.","authors":"Qichen Miao, Ruiqi Gao, Mingyang Huang, Guoqing Wang, Wengang Wang, Ming Luo","doi":"10.1038/s41413-026-00578-6","DOIUrl":"https://doi.org/10.1038/s41413-026-00578-6","url":null,"abstract":"<p><p>Biomolecular condensates are membraneless assemblies that concentrate proteins, nucleic acids, and other biomolecules into dynamic cellular compartments. Liquid-liquid phase separation (LLPS) is one important route by which such condensates form, particularly when multivalent interactions generate liquid-like, reversible assemblies. However, not every condensate or disease-associated assembly should be explained solely by LLPS. In the musculoskeletal system, condensates have been linked to transcription, signal transduction, RNA metabolism, stress responses, tissue development, homeostasis, and mechanoadaptation. Genetic mutations, altered post-translational modifications, and environmental stress can disturb these assemblies, but the evidence does not always establish whether condensates are causal drivers of disease or downstream responses to injury. This review examines how biomolecular condensates and LLPS-related mechanisms have been implicated in osteoporosis, osteoarthritis, skeletal muscle atrophy, bone and soft tissue sarcomas, and neuromusculoskeletal diseases. We focus on the strength of the available evidence, distinguish correlative observations from causal mechanisms where possible, and discuss how condensates may connect non-coding genetic variants, mechanical cues, metabolic signals, and disease phenotypes. We also assess the translational potential and limitations of condensate-based biomarkers, therapies that target pathological condensates, and phase-separation-inspired delivery systems. A central message is that biomolecular condensates offer a useful framework for musculoskeletal biology, but clinical translation will require disease-specific targets, human-relevant models, selective delivery, and rigorous tests of causality.</p>","PeriodicalId":9134,"journal":{"name":"Bone Research","volume":"14 1","pages":""},"PeriodicalIF":20.1,"publicationDate":"2026-08-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13484489/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148788077","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":"The sixth sense of the brain: interoception in organoid study.","authors":"Jilong Li, Fuxiao Wang, Qianmin Gao, Xiao Chen, Long Bai, Jiacan Su","doi":"10.1038/s41413-026-00569-7","DOIUrl":"https://doi.org/10.1038/s41413-026-00569-7","url":null,"abstract":"<p><p>Interoception is the process by which the nervous system senses, integrates, and interprets signals arising from within the body, thereby enabling the brain to monitor and regulate physiological functions. Often described as a \"sixth sense\", interoception links internal physiological states to brain-mediated homeostatic control, whereas sight, smell, hearing, taste, and touch primarily convey information from the external environment. Organoids are three-dimensional tissue models derived from stem or progenitor cells that reproduce selected structural and functional features of native organs. Because organoids are increasingly used in disease modeling, drug testing, and regenerative research, their integration with neural, endocrine, immune, and vascular components offers an opportunity to investigate brain-body communication. Conversely, organoid-based systems may provide experimentally tractable models for interoception. This review defines interoception and organoid technologies, examines brain-centered communication with skeletal and intestinal systems, and discusses how brain, bone, and intestinal organoids and assembloids could advance interoception research. In particular, organoid-based models may enable mechanistic investigation of neuroendocrine pathways, including the hypothalamic-pituitary-adrenal (HPA) axis, and thereby provide new insights into physiological regulation and disease progression.</p>","PeriodicalId":9134,"journal":{"name":"Bone Research","volume":"14 1","pages":""},"PeriodicalIF":20.1,"publicationDate":"2026-08-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13482827/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148788103","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":"Skeletal interoception regulates joint homeostasis and PGE2-induced pain: implication of disease-modifying treatment.","authors":"Qimiao Hu, Bonuo Qi, Yue Dong, Yushuang Pan, Yingjun Liu, Zhineng Chen, Jianqiao Fang, Yi Liang, Peng Zhang","doi":"10.1038/s41413-026-00561-1","DOIUrl":"https://doi.org/10.1038/s41413-026-00561-1","url":null,"abstract":"<p><p>Interoception is a core process through which the body perceives its internal state and regulates physiological homeostasis via bidirectional communication between the central and peripheral nervous system. Skeletal interoception is a specific circuitry for the brain control of the weight-bearing system, particularly responsible for sensing bone-derived internal signals to maintain skeletal homeostasis in response to mechanical loading. Recent studies uncovered that prostaglandin E2 (PGE2) plays a crucial role in skeletal interoception, and is therefore involved in major skeletal disorders and pain conditions such as low back pain, osteoarthritis and particularly ankle osteoarthritis (AOA). Ankle pain is clinically common, with a prevalence of 9%-15% among adults, severely impairing work productivity and quality of life. This article reviews the progress of skeletal interoception in skeletal pathogenesis and pain, with AOA as an example. Specifically, it discusses PGE2 and skeletal interoception in relation to pain and inflammation. We also attempted to interpret non-steroidal anti-inflammatory drugs (NSAIDs), surgical interventions and Traditional Chinese Medicine (TCM) therapies, especially acupuncture and electroacupuncture, in the therapy of pain and osteoarthritis from the viewpoint of skeletal interoception. Interoception is an emerging science in understanding how the brain regulates peripheral organs. Skeletal interoception mediated by PGE2 provides an opportunity to understand the potential of NSAIDs and acupuncture in regulating interoception for the treatment of skeletal disorders including ankle pain.</p>","PeriodicalId":9134,"journal":{"name":"Bone Research","volume":"14 1","pages":""},"PeriodicalIF":20.1,"publicationDate":"2026-08-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13473667/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148764226","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":"Expert consensus on osteoporosis risk management in patients with sleep disorders.","authors":"Siqi Leng, Jinming Yang, Yuming Jin, Jie Shi, Ye Zhang, Junying Zhou, Lu Tan, Taomei Li, Peiyan Ni, Kejia Hu, Yuan Shi, Jiamin Liao, Yun Li, Pei Xue, Christian Benedict, Alexandros N Vgontzas, Michael Furian, Talant Sooronbaev, Naima Covassin, Virend K Somers, Zhoulong Yu, Hongqiang Sun, Xiao Tan, Jihui Zhang, Yun Kwok Wing, Yue Leng, Larry D Sanford, Michael V Vitiello, Katie L Stone, Rong Ren, Lin Lu, Xiangdong Tang","doi":"10.1038/s41413-026-00562-0","DOIUrl":"10.1038/s41413-026-00562-0","url":null,"abstract":"<p><p>A rate-limiting step in the prevention and early intervention of osteoporosis is identifying its asymptomatic onset. Accumulating evidence shows that sleep disorders are associated with an increased risk of osteoporosis. Given their early detectable and modifiable nature, integrating sleep disorder management into osteoporosis prevention and care pathways offers a novel approach for enhancing skeletal health. This expert consensus represents a collaborative effort by specialists in sleep medicine and orthopedics from across the world, integrating epidemiological, mechanistic, and interventional evidence to provide general guidance for prevention and clinical practice, and to foster multidisciplinary collaboration in the management of sleep disorders and osteoporosis.</p>","PeriodicalId":9134,"journal":{"name":"Bone Research","volume":"14 1","pages":""},"PeriodicalIF":20.1,"publicationDate":"2026-08-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13473140/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148757559","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":"Youthfulness of marrow Adipoq⁺ cells maintained by Cbfβ facilitates stem cell-based bone repair.","authors":"Tiannan Huang, Shali Wu, Wei Qian, Ruiying Chen, Erman Chen, Meizhu Wang, Cui Zhang, Chenhe Zhou, Luyang Yu, Mengjie Wu, Yi-Ping Li, Mengrui Wu","doi":"10.1038/s41413-026-00568-8","DOIUrl":"10.1038/s41413-026-00568-8","url":null,"abstract":"<p><p>Exhaustion of skeletal stem and progenitor cells (SSPCs) drives age-related delays in fracture repair, yet the upstream regulators of SSPC maintenance are unclear. We identify that core-binding factor β (Cbfβ) in bone marrow Adipoq⁺ cells (BMACs) is essential for maintaining SSPC number and function. Cbfβ deletion in BMACs (CKO) leads to SSPC depletion, including periosteal populations, and impairs bicortical fracture healing in mice. Multi-omics (RNA-seq, CUT&Tag-seq, and ATAC-seq) reveal that Cbfβ preserves chromatin accessibility at DNA repair loci, maintaining genomic stability, preventing BMAC senescence, and mitigating the senescence-associated secretory phenotype (SASP). Senolytic therapy alleviates BMAC senescence, restores SSPC populations, and improves bone repair in CKO mice. In both humans and mice, Cbfβ expression declines with aging, accompanied by increased BMAC senescence. AAV-mediated Cbfβ overexpression restores aging-related bone repair and SSPC decline. These findings reveal a novel mechanism in which Cbfβ in BMACs regulates SSPC maintenance via a senescence/SASP axis, offering a potential therapeutic strategy for age-related bone repair deficits.</p>","PeriodicalId":9134,"journal":{"name":"Bone Research","volume":"14 1","pages":""},"PeriodicalIF":20.1,"publicationDate":"2026-08-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13458481/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148705325","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":"Human growth plates house resting zone sub-populations with features of quiescent stem cells.","authors":"Mahtab Avijgan, Ana R López-Pérez, Leire Alonso Galicia, Jose G Marchan-Alvarez, Laura Sudupe, Ruihan Zhou, Amal Nazaraliyev, Žaneta Andrusivová, Ludvig Larsson, Pâmella Miranda, Doste R Mamand, Yunhan Zhao, Farasat Zaman, Hong Qian, Klas Blomgren, Felipe Prosper, Oscar P B Wiklander, Jesper N Tegner, Joakim Lundeberg, Lars Sävendahl, Reza Mirzazadeh, David Gomez-Cabrero, Phillip T Newton","doi":"10.1038/s41413-026-00564-y","DOIUrl":"10.1038/s41413-026-00564-y","url":null,"abstract":"<p><p>Maintaining postnatal bone growth is crucial for humans to reach their final height. To determine transcriptional networks coordinating this process, we applied spatially resolved transcriptomics to growth plate biopsies obtained from healthy adolescents who underwent epiphysiodesis surgery for idiopathic tall stature. Spatial profiling revealed new markers for each zone of the human growth plate and identified genes associated with poorly understood growth disorders, including the novel hypertrophic zone marker SGMS2. We elaborated on this finding and established that Sgms2 is present in growth plate-derived matrix vesicles, and its activity facilitates mineralization - a process impaired in patients with SGMS2 mutations. By exploring the low transcriptional activity of resting zone chondrocytes, we found that a subset of these cells exists in a functionally quiescent state in vivo, as determined by their predominantly nuclear mRNA, abundant heterochromatin, and ability to exit the G0 phase under specific conditions - features shared with skeletal stem cells in mouse growth plates. Additionally, we identified distinct sub-populations of human resting zone chondrocytes; an exploration of their hierarchy determined that CHRDL2 and/or SFRP5-positive sub-populations were among the least quiescent resting zone cells. In summary, we generated a comprehensive map of gene expression within the human growth plate, revealing novel zone-specific markers, new primary growth disorders, candidate pharmacological targets, and sub-populations of resting zone chondrocytes with features of quiescent stem cells. These results contribute to a better understanding of the cellular and molecular mechanisms governing human height and can facilitate improved diagnosis and treatment strategies for patients with skeletal growth disorders.</p>","PeriodicalId":9134,"journal":{"name":"Bone Research","volume":"14 1","pages":""},"PeriodicalIF":20.1,"publicationDate":"2026-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13438842/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148677076","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":"Inflammation driven by NF-ĸB compromises bone formation by inducing the differentiation of osteoblasts into atypical inflammatory osteocyte-like cells.","authors":"Gaurav Swarnkar, Md Fahim Ahmad, Marwa Zeyad, Abdul Malik Tyagi, Musarrat Naaz, Gabriel Mbalaviele, Yousef Abu-Amer","doi":"10.1038/s41413-026-00546-0","DOIUrl":"10.1038/s41413-026-00546-0","url":null,"abstract":"<p><p>Inflammation causes bone loss by dysregulating the differentiation and functions of osteoclasts, osteoblasts, and osteocytes. This process can be modeled by the expression of constitutively activated IKK2 (IKK2ca), a strategy that we leveraged to investigate the mechanisms through which inflammation negatively affects cells of the osteoblast/osteocyte lineage. We found that mice expressing IKK2ca in osteoblasts exhibit significant bone loss. Mechanistically, IKK2ca downregulates the expression of osteoblast genes while inducing the differentiation of bone-forming osteoblasts into catabolic osteocytes like cells, expressing high levels of Podoplanin, Fgf23, Dkk1 and Sclerostin. We term these atypical inflammatory osteocyte-like cells (aiOCy-L cells) as they highly express inflammatory and senescence markers and promote osteoclast differentiation as well. Additional data show that inflammation induces abnormal differentiation of OB into aiOCy-L cells through upregulating mTOR and glycolysis. In summary, we uncovered a mechanism by which inflammation alters osteoblast differentiation and fate decision via the IKK2/mTOR/glycolysis axis.</p>","PeriodicalId":9134,"journal":{"name":"Bone Research","volume":"14 1","pages":""},"PeriodicalIF":20.1,"publicationDate":"2026-08-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13439236/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148677035","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":"IGSF10 regulates osteogenesis and osteoclastogenesis via a noncanonical EGFR-STAT1 signaling axis to promote skeletal regeneration.","authors":"Jin Wen, Yuwei Deng, Ruixue Jiang, Longwei Hu, Qianju Wu, Xiao Wang, Zheting Liao, Wenjing Ding, Fei Jiang, Xi Chen, Xiaohan Ma, Chunhua Yu, Xinquan Jiang","doi":"10.1038/s41413-026-00552-2","DOIUrl":"10.1038/s41413-026-00552-2","url":null,"abstract":"<p><p>Bone remodeling requires precise coordination between osteoblast-mediated bone formation and osteoclast-driven resorption. However, directly targetable and therapeutically actionable mediators that can coordinately modulate both processes during regeneration remain relatively limited. Here, we identify immunoglobulin superfamily member 10 (IGSF10) as a dual-function modulator of bone remodeling. Igsf10-deficient mice exhibit reduced bone mass, elevated osteoclast activity, and impaired osteogenesis. Recombinant IGSF10 protein restores osteogenic capacity and suppresses osteoclastogenesis in knockout cells, while exerting pro-osteogenic and anti-resorptive effects in wild-type mesenchymal and monocyte-derived cultures. Mechanistically, IGSF10 activates a noncanonical EGFR-STAT1 signaling pathway, distinct from BMP2-Smad signaling. Co-immunoprecipitation and molecular docking confirm IGSF10-EGFR interaction, and blockade of EGFR abrogates IGSF10-induced osteogenesis and its inhibitory effects on osteoclastogenesis. In vivo, IGSF10 promotes bone regeneration in both calvarial and periodontal defect models and exhibits synergy with subtherapeutic BMP2. These findings position IGSF10 as a previously unrecognized dual-acting regulator that coordinates bone formation and resorption in a context-dependent manner, with potential therapeutic value for craniofacial and skeletal regeneration.</p>","PeriodicalId":9134,"journal":{"name":"Bone Research","volume":"14 1","pages":""},"PeriodicalIF":20.1,"publicationDate":"2026-08-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13438563/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148677108","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":"Apoptosis of Mdm2-deficient osteocytes enhances osteogenesis through TRPM8-enriched apoptotic vesicles.","authors":"Xin Liu, Huiwen Zheng, Aochen Wang, Jianing Liu, Zhi Chen, Yiping Chen, Guobin Yang, Di Chen, Yufeng Zhang, Guohua Yuan","doi":"10.1038/s41413-026-00570-0","DOIUrl":"10.1038/s41413-026-00570-0","url":null,"abstract":"<p><p>During homeostasis, osteocyte apoptosis is typically associated with bone loss through enhanced osteoclast recruitment and bone resorption. However, whether apoptotic osteocytes also regulate bone formation remains elusive. Here we report that conditional deletion of Mdm2, an E3 ubiquitin ligase regulating cell survival, causes osteocyte apoptosis but paradoxically results in a marked increase in bone mass attributed to up-regulated osteogenic activity. Single-cell RNA sequencing reveals enhanced osteoblastic differentiation of bone marrow mesenchymal stem cells (BMSCs) in conditional knockout mice, with enrichment of cellular calcium related pathways. Mechanistically, apoptotic vesicles (apovs) from Mdm2-deleted osteocytes are engulfed by BMSCs. TRPM8, a calcium channel protein, is enriched in osteocyte-derived apovs and transported into BMSCs, thereby promoting osteoblastic differentiation. Additionally, pharmacological inhibition of TRPM8 attenuates the high bone mass phenotype in conditional knockout mice. Therefore, Mdm2 deletion in osteocytes leads to osteocyte apoptosis, which enhances bone formation through communicating with BMSCs via TRPM8-enriched apovs. Our findings underscore the pivotal role of osteocytes in bone homeostasis and unveil a previously unrecognized mechanism whereby osteocyte apoptosis stimulates osteogenesis through affecting the fate of BMSCs in a TRPM8-mediated paracrine mechanism.</p>","PeriodicalId":9134,"journal":{"name":"Bone Research","volume":"14 1","pages":""},"PeriodicalIF":20.1,"publicationDate":"2026-08-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13429674/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148663336","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":"DMP1-Cre expressing cells mediate the gain in bone mass and strength, but not the increase in bone remodeling, induced by ligands of the parathyroid hormone receptor","authors":"Nisreen Akel, Sasidhar Uppuganti, Jeff D. Thostenson, Wyatt House, Kaitlyn Hapke, Gretel G. Pellegrini, Joan Pizarro-Gómez, Shenyang Li, Meloney Cregor, Silvia Marino, Jeffry S. Nyman, Teresita Bellido","doi":"10.1038/s41413-026-00555-z","DOIUrl":"https://doi.org/10.1038/s41413-026-00555-z","url":null,"abstract":"Signaling downstream of the receptor of parathyroid hormone (PTH1R) exerts two major skeletal effects: increases bone remodeling and, when stimulated intermittently, induces bone anabolism. Osteocytes express the PTH1R and are critical for the action of teriparatide/parathyroid hormone 1–34 (PTH). However, it is unknown whether they also mediate the effects of abaloparatide (a 34 amino acid synthetic analog of human parathyroid hormone-related protein, ABL), and whether actions on osteocytes are required for the increase in remodeling and/or the bone gain induced by PTH/ABL in diabetes. We addressed these questions by treating with PTH or ABL control or diabetic (DM) mice lacking the PTH1R in DMP1-Cre expressing cells that targets all osteocytes (cKO). Both PTH and ABL increased bone mass and improved or corrected cortical and trabecular bone microarchitecture only in fl/fl littermates but not in cKO, control or DM mice. Further, PTH/ABL increased bone strength and microindentation resistance only in control or DM fl/fl mice. In contrast, PTH/ABL increased serum P1NP and bone formation on cancellous, periosteal and endocortical surfaces, in control or DM mice of both genotypes. Moreover, serum CTX and osteoclast surface were increased by PTH/ABL in fl/fl and cKO, control or DM mice. Thus, actions on DMP1-Cre expressing cells are required for bone gain, microarchitecture restoration, strength and resistance to fracture, exerted by PTH and ABL under physiological and DM conditions, but not for the increase in bone remodeling. These findings demonstrate the dissociation of bone gain from bone remodeling and reveal that actions on DMP1-Cre expressing cells drive the gain in bone mass and strength induced by PTH and ABL.","PeriodicalId":9134,"journal":{"name":"Bone Research","volume":"11 1","pages":""},"PeriodicalIF":12.7,"publicationDate":"2026-07-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148612706","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}