Bone Research最新文献

Advances in spatial transcriptomics and its application in the musculoskeletal system 空间转录组学研究进展及其在肌肉骨骼系统中的应用

IF 12.7 1区医学

Bone Research Pub Date : 2025-05-16 DOI: 10.1038/s41413-025-00429-w

Haoyu Wang, Peng Cheng, Juan Wang, Hongzhi Lv, Jie Han, Zhiyong Hou, Ren Xu, Wei Chen

{"title":"Advances in spatial transcriptomics and its application in the musculoskeletal system","authors":"Haoyu Wang, Peng Cheng, Juan Wang, Hongzhi Lv, Jie Han, Zhiyong Hou, Ren Xu, Wei Chen","doi":"10.1038/s41413-025-00429-w","DOIUrl":"https://doi.org/10.1038/s41413-025-00429-w","url":null,"abstract":"While bulk RNA sequencing and single-cell RNA sequencing have shed light on cellular heterogeneity and potential molecular mechanisms in the musculoskeletal system in both physiological and various pathological states, the spatial localization of cells and molecules and intercellular interactions within the tissue context require further elucidation. Spatial transcriptomics has revolutionized biological research by simultaneously capturing gene expression profiles and in situ spatial information of tissues, gradually finding applications in musculoskeletal research. This review provides a summary of recent advances in spatial transcriptomics and its application to the musculoskeletal system. The classification and characteristics of data acquisition techniques in spatial transcriptomics are briefly outlined, with an emphasis on widely-adopted representative technologies and the latest technological breakthroughs, accompanied by a concise workflow for incorporating spatial transcriptomics into musculoskeletal system research. The role of spatial transcriptomics in revealing physiological mechanisms of the musculoskeletal system, particularly during developmental processes, is thoroughly summarized. Furthermore, recent discoveries and achievements of this emerging omics tool in addressing inflammatory, traumatic, degenerative, and tumorous diseases of the musculoskeletal system are compiled. Finally, challenges and potential future directions for spatial transcriptomics, both as a field and in its applications in the musculoskeletal system, are discussed.","PeriodicalId":9134,"journal":{"name":"Bone Research","volume":"124 1","pages":""},"PeriodicalIF":12.7,"publicationDate":"2025-05-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144066200","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}

引用次数: 0

PTPN11 in cartilage development, adult homeostasis, and diseases PTPN11在软骨发育、成人体内平衡和疾病中的作用

IF 12.7 1区医学

Bone Research Pub Date : 2025-05-16 DOI: 10.1038/s41413-025-00425-0

Wentian Yang, Véronique Lefebvre

{"title":"PTPN11 in cartilage development, adult homeostasis, and diseases","authors":"Wentian Yang, Véronique Lefebvre","doi":"10.1038/s41413-025-00425-0","DOIUrl":"https://doi.org/10.1038/s41413-025-00425-0","url":null,"abstract":"The SH2 domain-containing protein tyrosine phosphatase 2 (SHP2, also known as PTP2C), encoded by PTPN11, is ubiquitously expressed and has context-specific effects. It promotes RAS/MAPK signaling downstream of receptor tyrosine kinases, cytokine receptors, and extracellular matrix proteins, and was shown in various lineages to modulate cell survival, proliferation, differentiation, and migration. Over the past decade, PTPN11 inactivation in chondrocytes was found to cause metachondromatosis, a rare disorder characterized by multiple enchondromas and osteochondroma-like lesions. Moreover, SHP2 inhibition was found to mitigate osteoarthritis pathogenesis in mice, and abundant but incomplete evidence suggests that SHP2 is crucial for cartilage development and adult homeostasis, during which its expression and activity are tightly regulated transcriptionally and posttranslationally, and by varying sets of functional partners. Fully uncovering SHP2 actions and regulation in chondrocytes is thus fundamental to understanding the mechanisms underlying both rare and common cartilage diseases and to designing effective disease treatments. We here review current knowledge, highlight recent discoveries and controversies, and propose new research directions to answer remaining questions.","PeriodicalId":9134,"journal":{"name":"Bone Research","volume":"2 1","pages":""},"PeriodicalIF":12.7,"publicationDate":"2025-05-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144066197","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}

引用次数: 0

Biased agonism of G protein-coupled receptors as a novel strategy for osteoarthritis therapy G蛋白偶联受体的偏向激动作用作为骨关节炎治疗的新策略

IF 12.7 1区医学

Bone Research Pub Date : 2025-05-12 DOI: 10.1038/s41413-025-00435-y

Xiangbo Meng, Ling Qin, Xinluan Wang

{"title":"Biased agonism of G protein-coupled receptors as a novel strategy for osteoarthritis therapy","authors":"Xiangbo Meng, Ling Qin, Xinluan Wang","doi":"10.1038/s41413-025-00435-y","DOIUrl":"https://doi.org/10.1038/s41413-025-00435-y","url":null,"abstract":"Osteoarthritis (OA) is a prevalent degenerative joint disorder marked by chronic pain, inflammation, and cartilage loss, with current treatments limited to symptom relief. G protein-coupled receptors (GPCRs) play a pivotal role in OA progression by regulating inflammation, chondrocyte survival, and matrix homeostasis. However, their multifaceted signaling, via G proteins or β-arrestins, poses challenges for precise therapeutic targeting. Biased agonism, where ligands selectively activate specific GPCR pathways, emerges as a promising approach to optimize efficacy and reduce side effects. This review examines biased signaling in OA-associated GPCRs, including cannabinoid receptors (CB1, CB2), chemokine receptors (CCR2, CXCR4), protease-activated receptors (PAR-2), adenosine receptors (A1R, A2AR, A2BR, A3R), melanocortin receptors (MC1R, MC3R), bradykinin receptors (B2R), prostaglandin E2 receptors (EP-2, EP-4), and calcium-sensing receptors (CaSR). We analyze ligands in clinical trials and explore natural products from Traditional Chinese Medicine as potential biased agonists. These compounds, with diverse structures and bioactivities, offer novel therapeutic avenues. By harnessing biased agonism, this review underscores the potential for developing targeted, safer OA therapies that address its complex pathology, bridging molecular insights with clinical translation.","PeriodicalId":9134,"journal":{"name":"Bone Research","volume":"1 1","pages":""},"PeriodicalIF":12.7,"publicationDate":"2025-05-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143933586","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}

引用次数: 0

IGF2BP3-mediated m6A modification of RASGRF1 promoting joint injury in rheumatoid arthritis igf2bp3介导的m6A修饰促进类风湿性关节炎关节损伤

IF 12.7 1区医学

Bone Research Pub Date : 2025-05-12 DOI: 10.1038/s41413-025-00434-z

Qishun Geng, Yi Jiao, Wenya Diao, Jiahe Xu, Zhaoran Wang, Xing Wang, Zihan Wang, Lu Zhao, Lei Yang, Yilin Wang, Tingting Deng, Bailiang Wang, Cheng Xiao

{"title":"IGF2BP3-mediated m6A modification of RASGRF1 promoting joint injury in rheumatoid arthritis","authors":"Qishun Geng, Yi Jiao, Wenya Diao, Jiahe Xu, Zhaoran Wang, Xing Wang, Zihan Wang, Lu Zhao, Lei Yang, Yilin Wang, Tingting Deng, Bailiang Wang, Cheng Xiao","doi":"10.1038/s41413-025-00434-z","DOIUrl":"https://doi.org/10.1038/s41413-025-00434-z","url":null,"abstract":"With the deepening of epigenetic research, studies have shown that N6-methyladenosine (m6A) is closely related to the development of rheumatoid arthritis (RA), but the mechanism is still unclear. In the study, we collected synovial tissues from normal controls and patients with osteoarthritis (OA) or RA. The levels of m6A and inflammation were analyzed by immunofluorescence staining and western blotting. The roles of IGF2BP3 in cell proliferation and inflammatory activation were explored using transfection and RNA immunoprecipitation assays. IGF2BP3−/− mice were generated and used to establish an arthritis mouse model by transferring serum from adult arthritis K/BxN mice. We found m6A levels were markedly increased in RA patients and mouse models, and the expression of IGF2BP3 was upregulated in individuals with RA and related to the levels of inflammatory markers. IGF2BP3 played an important part in RA-fibroblast-like synoviocytes (FLS) by promoting cell proliferation, migration, invasion, inflammatory cytokine release and inhibiting autophagy. In addition, IGF2BP3 inhibited autophagy to reduce ROS production, thereby decreasing the inflammatory activation of macrophages. More importantly, RASGRF1-mediated mTORC1 activation played a crucial role in the ability of IGF2BP3 to promote cell proliferation and inflammatory activation. In an arthritis model of IGF2BP3−/− mice, IGF2BP3 knockout inhibited RA-FLS proliferation and inflammatory infiltration, and further ameliorated RA joint injury. Our study revealed an important role for IGF2BP3 in RA progression. The targeted inhibition of IGF2BP3 reduced cell proliferation and inflammatory activation and limited RA development, providing a potential strategy for RA therapy.","PeriodicalId":9134,"journal":{"name":"Bone Research","volume":"119 1","pages":""},"PeriodicalIF":12.7,"publicationDate":"2025-05-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143933590","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}

引用次数: 0

Sirt6 deficiency promotes senescence and age-associated intervertebral disc degeneration in mice Sirt6缺乏促进小鼠衰老和与年龄相关的椎间盘退变

IF 12.7 1区医学

Bone Research Pub Date : 2025-05-08 DOI: 10.1038/s41413-025-00422-3

Pranay Ramteke, Bahiyah Watson, Mallory Toci, Victoria A. Tran, Shira Johnston, Maria Tsingas, Ruteja A. Barve, Ramkrishna Mitra, Richard F. Loeser, John A. Collins, Makarand V. Risbud

{"title":"Sirt6 deficiency promotes senescence and age-associated intervertebral disc degeneration in mice","authors":"Pranay Ramteke, Bahiyah Watson, Mallory Toci, Victoria A. Tran, Shira Johnston, Maria Tsingas, Ruteja A. Barve, Ramkrishna Mitra, Richard F. Loeser, John A. Collins, Makarand V. Risbud","doi":"10.1038/s41413-025-00422-3","DOIUrl":"https://doi.org/10.1038/s41413-025-00422-3","url":null,"abstract":"Intervertebral disc degeneration is a major risk factor contributing to chronic low back and neck pain. While the etiological factors for disc degeneration vary, age is still one of the most important risk factors. Recent studies have shown the promising role of SIRT6 in mammalian aging and skeletal tissue health, however its role in the intervertebral disc health remains unexplored. We investigated the contribution of SIRT6 to disc health by studying the age-dependent spinal phenotype of mice with conditional deletion of Sirt6 in the disc (AcanCreERT2; Sirt6fl/fl). Histological studies showed a degenerative phenotype in knockout mice compared to Sirt6fl/fl control mice at 12 months, which became pronounced at 24 months. RNA-Seq analysis of NP and AF tissues, in vitro quantitative histone analysis, and RNA-seq with ATAC-seq multiomic studies revealed that SIRT6-loss resulted in changes in acetylation and methylation status of specific Histone 3 lysine residues and affected DNA accessibility and transcriptomic landscape. A decrease in autophagy and an increase in DNA damage were also noted in Sirt6-deficient cells. Further mechanistic insights revealed that loss of SIRT6 increased senescence and SASP burden in the disc characterized by increased p21, p19, γH2AX, IL-6, IL-1β, and TGF-β abundance. Taken together, our study highlights the contribution of SIRT6 in modulating DNA damage, autophagy, and cell senescence and its importance in maintaining disc health during aging, thereby underscoring it as a potential therapeutic target to treat intervertebral disc degeneration.","PeriodicalId":9134,"journal":{"name":"Bone Research","volume":"53 1","pages":""},"PeriodicalIF":12.7,"publicationDate":"2025-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143920251","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}

引用次数: 0

Bone-derived factors mediate crosstalk between skeletal and extra-skeletal organs 骨源性因子介导骨骼和骨骼外器官之间的串扰

IF 12.7 1区医学

Bone Research Pub Date : 2025-04-30 DOI: 10.1038/s41413-025-00424-1

Tailin He, Lei Qin, Sheng Chen, Shaochuan Huo, Jie Li, Fuping Zhang, Weihong Yi, Yifang Mei, Guozhi Xiao

{"title":"Bone-derived factors mediate crosstalk between skeletal and extra-skeletal organs","authors":"Tailin He, Lei Qin, Sheng Chen, Shaochuan Huo, Jie Li, Fuping Zhang, Weihong Yi, Yifang Mei, Guozhi Xiao","doi":"10.1038/s41413-025-00424-1","DOIUrl":"https://doi.org/10.1038/s41413-025-00424-1","url":null,"abstract":"Bone has long been acknowledged as a fundamental structural entity that provides support and protection to the body’s organs. However, emerging research indicates that bone plays a crucial role in the regulation of systemic metabolism. This is achieved through the secretion of a variety of hormones, cytokines, metal ions, extracellular vesicles, and other proteins/peptides, collectively referred to as bone-derived factors (BDFs). BDFs act as a medium through which bones can exert targeted regulatory functions upon various organs, thereby underscoring the profound and concrete implications of bone in human physiology. Nevertheless, there remains a pressing need for further investigations to elucidate the underlying mechanisms that inform the effects of bone on other body systems. This review aims to summarize the current findings related to the roles of these significant modulators across different organs and metabolic contexts by regulating critical genes and signaling pathways in vivo. It also addresses their involvement in the pathogenesis of various diseases affecting the musculoskeletal system, circulatory system, glucose and lipid metabolism, central nervous system, urinary system, and reproductive system. The insights gained from this review may contribute to the development of innovative therapeutic strategies through a focused approach to bone secretomes. Continued research into BDFs is expected to enhance our understanding of bone as a multifunctional organ with diverse regulatory roles in human health.","PeriodicalId":9134,"journal":{"name":"Bone Research","volume":"43 1","pages":""},"PeriodicalIF":12.7,"publicationDate":"2025-04-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143889591","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}

引用次数: 0

Advancing osteoarthritis research: the role of AI in clinical, imaging and omics fields 推进骨关节炎研究：人工智能在临床、成像和海洋学领域的作用

IF 12.7 1区医学

Bone Research Pub Date : 2025-04-22 DOI: 10.1038/s41413-025-00423-2

Jingfeng Ou, Jin Zhang, Momen Alswadeh, Zhenglin Zhu, Jijun Tang, Hongxun Sang, Ke Lu

{"title":"Advancing osteoarthritis research: the role of AI in clinical, imaging and omics fields","authors":"Jingfeng Ou, Jin Zhang, Momen Alswadeh, Zhenglin Zhu, Jijun Tang, Hongxun Sang, Ke Lu","doi":"10.1038/s41413-025-00423-2","DOIUrl":"https://doi.org/10.1038/s41413-025-00423-2","url":null,"abstract":"Osteoarthritis (OA) is a degenerative joint disease with significant clinical and societal impact. Traditional diagnostic methods, including subjective clinical assessments and imaging techniques such as X-rays and MRIs, are often limited in their ability to detect early-stage OA or capture subtle joint changes. These limitations result in delayed diagnoses and inconsistent outcomes. Additionally, the analysis of omics data is challenged by the complexity and high dimensionality of biological datasets, making it difficult to identify key molecular mechanisms and biomarkers. Recent advancements in artificial intelligence (AI) offer transformative potential to address these challenges. This review systematically explores the integration of AI into OA research, focusing on applications such as AI-driven early screening and risk prediction from electronic health records (EHR), automated grading and morphological analysis of imaging data, and biomarker discovery through multi-omics integration. By consolidating progress across clinical, imaging, and omics domains, this review provides a comprehensive perspective on how AI is reshaping OA research. The findings have the potential to drive innovations in personalized medicine and targeted interventions, addressing longstanding challenges in OA diagnosis and management.","PeriodicalId":9134,"journal":{"name":"Bone Research","volume":"6 1","pages":""},"PeriodicalIF":12.7,"publicationDate":"2025-04-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143857471","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}

引用次数: 0

SPI1 activates mitochondrial unfolded response signaling to inhibit chondrocyte senescence and relieves osteoarthritis SPI1激活线粒体未折叠反应信号，抑制软骨细胞衰老，缓解骨关节炎

IF 12.7 1区医学

Bone Research Pub Date : 2025-04-14 DOI: 10.1038/s41413-025-00421-4

Xiangyu Zu, Shenghong Chen, Zhengyuan Li, Lin Hao, Wenhan Fu, Hui Zhang, Zongsheng Yin, Yin Wang, Jun Wang

{"title":"SPI1 activates mitochondrial unfolded response signaling to inhibit chondrocyte senescence and relieves osteoarthritis","authors":"Xiangyu Zu, Shenghong Chen, Zhengyuan Li, Lin Hao, Wenhan Fu, Hui Zhang, Zongsheng Yin, Yin Wang, Jun Wang","doi":"10.1038/s41413-025-00421-4","DOIUrl":"https://doi.org/10.1038/s41413-025-00421-4","url":null,"abstract":"Chondrocyte senescence is a critical pathological hallmark of osteoarthritis (OA). Aberrant mechanical stress is considered a pivotal determinant in chondrocyte aging; however, the precise underlying mechanism remains elusive. Our findings demonstrate that SPI1 plays a significant role in counteracting chondrocyte senescence and inhibiting OA progression. SPI1 binds to the PERK promoter, thereby promoting its transcriptional activity. Importantly, PERK, rather than GCN2, facilitates eIF2α phosphorylation, activating the mitochondrial unfolded protein response (UPRmt) and impeding chondrocyte senescence. Deficiency of SPI1 in mechanical overload-induced mice leads to diminished UPRmt activation and accelerated OA progression. Intra-articular injection of adenovirus vectors overexpressing SPI1 and PERK effectively mitigates cartilage degeneration. In summary, our study elucidates the crucial regulatory role of SPI1 in the pathogenesis of chondrocyte senescence by activating UPRmt signaling through PERK, which may present a novel therapeutic target for treating OA.<figure>SPI1 alleviates the progression of OA by inhibiting mechanical stress-induced chondrocyte senescence through mitochondrial UPR signaling.</figure>","PeriodicalId":9134,"journal":{"name":"Bone Research","volume":"40 1","pages":""},"PeriodicalIF":12.7,"publicationDate":"2025-04-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143827656","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}

引用次数: 0

NELL2, a novel osteoinductive factor, regulates osteoblast differentiation and bone homeostasis through fibronectin 1/integrin-mediated FAK/AKT signaling NELL2是一种新型的骨诱导因子，通过纤维连接蛋白1/整合素介导的FAK/AKT信号传导调节成骨细胞分化和骨稳态

IF 12.7 1区医学

Bone Research Pub Date : 2025-04-11 DOI: 10.1038/s41413-025-00420-5

Hairui Yuan, Xinyu Wang, Shuanglin Du, Mengyue Li, Endong Zhu, Jie Zhou, Yuan Dong, Shuang Wang, Liying Shan, Qian Liu, Baoli Wang

{"title":"NELL2, a novel osteoinductive factor, regulates osteoblast differentiation and bone homeostasis through fibronectin 1/integrin-mediated FAK/AKT signaling","authors":"Hairui Yuan, Xinyu Wang, Shuanglin Du, Mengyue Li, Endong Zhu, Jie Zhou, Yuan Dong, Shuang Wang, Liying Shan, Qian Liu, Baoli Wang","doi":"10.1038/s41413-025-00420-5","DOIUrl":"https://doi.org/10.1038/s41413-025-00420-5","url":null,"abstract":"Neural EGFL-like 2 (NELL2) is a secreted protein known for its regulatory functions in the nervous and reproductive systems, yet its role in bone biology remains unexplored. In this study, we observed that NELL2 was diminished in the bone of aged and ovariectomized (OVX) mice, as well as in the serum of osteopenia and osteoporosis patients. In vitro loss-of-function and gain-of-function studies revealed that NELL2 facilitated osteoblast differentiation and impeded adipocyte differentiation from stromal progenitor cells. In vivo studies further demonstrated that the deletion of NELL2 in preosteoblasts resulted in decreased cancellous bone mass in mice. Mechanistically, NELL2 interacted with the FNI-type domain located at the C-terminus of Fibronectin 1 (Fn1). Moreover, we found that NELL2 activated the focal adhesion kinase (FAK)/AKT signaling pathway through Fn1/integrin β1 (ITGB1), leading to the promotion of osteogenesis and the inhibition of adipogenesis. Notably, administration of NELL2-AAV was found to ameliorate bone loss in OVX mice. These findings underscore the significant role of NELL2 in osteoblast differentiation and bone homeostasis, suggesting its potential as a therapeutic target for managing osteoporosis.","PeriodicalId":9134,"journal":{"name":"Bone Research","volume":"16 1","pages":""},"PeriodicalIF":12.7,"publicationDate":"2025-04-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143819475","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}

引用次数: 0

Cell communication and relevant signaling pathways in osteogenesis–angiogenesis coupling 骨生成-血管生成耦合中的细胞通讯及相关信号通路

IF 12.7 1区医学

Bone Research Pub Date : 2025-04-07 DOI: 10.1038/s41413-025-00417-0

Shuqing Li, Xinjia Cai, Jiahe Guo, Xiaolu Li, Wen Li, Yan Liu, Mengchun Qi

{"title":"Cell communication and relevant signaling pathways in osteogenesis–angiogenesis coupling","authors":"Shuqing Li, Xinjia Cai, Jiahe Guo, Xiaolu Li, Wen Li, Yan Liu, Mengchun Qi","doi":"10.1038/s41413-025-00417-0","DOIUrl":"https://doi.org/10.1038/s41413-025-00417-0","url":null,"abstract":"Osteogenesis is the process of bone formation mediated by the osteoblasts, participating in various bone-related physiological processes including bone development, bone homeostasis and fracture healing. It exhibits temporal and spatial interconnectivity with angiogenesis, constructed by multiple forms of cell communication occurring between bone and vascular endothelial cells. Molecular regulation among different cell types is crucial for coordinating osteogenesis and angiogenesis to facilitate bone remodeling, fracture healing, and other bone-related processes. The transmission of signaling molecules and the activation of their corresponding signal pathways are indispensable for various forms of cell communication. This communication acts as a “bridge” in coupling osteogenesis to angiogenesis. This article reviews the modes and processes of cell communication in osteogenesis-angiogenesis coupling over the past decade, mainly focusing on interactions among bone-related cells and vascular endothelial cells to provide insights into the mechanism of cell communication of osteogenesis-angiogenesis coupling in different bone-related contexts. Moreover, clinical relevance and applications are also introduced in this review.","PeriodicalId":9134,"journal":{"name":"Bone Research","volume":"38 1","pages":""},"PeriodicalIF":12.7,"publicationDate":"2025-04-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143790156","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}

引用次数: 0