Mechanobiology in Medicine最新文献

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Mechanosensitive nuclear checkpoint: nuclear envelope as a sensor of chromosomal instability and driver of cell fate 机械敏感核检查点:核包膜作为染色体不稳定性的传感器和细胞命运的驱动因素
Mechanobiology in Medicine Pub Date : 2025-06-01 Epub Date: 2025-05-21 DOI: 10.1016/j.mbm.2025.100135
Chenyang Ji, Junwei Chen, Fuxiang Wei
{"title":"Mechanosensitive nuclear checkpoint: nuclear envelope as a sensor of chromosomal instability and driver of cell fate","authors":"Chenyang Ji,&nbsp;Junwei Chen,&nbsp;Fuxiang Wei","doi":"10.1016/j.mbm.2025.100135","DOIUrl":"10.1016/j.mbm.2025.100135","url":null,"abstract":"<div><div>The nuclear envelope (NE) is a dynamic, mechanosensitive structure that functions as a protective barrier for the genome and serves as a checkpoint responding to external stimuli. It plays a critical role in maintaining genomic stability and regulating cell fate. This review synthesizes recent research highlighting the role of NE as a mechanical checkpoint in ensuring accurate chromosome segregation, regulating cell cycle progression, and contributing to cancer development. Chromosome mis-segregation during cell division is a major driver of aneuploidy, a condition closely associated with genomic instability and cellular transformation. The role of NE in chromatin organization and gene expression regulation is also discussed, underscoring its importance in cell differentiation and identity.</div></div>","PeriodicalId":100900,"journal":{"name":"Mechanobiology in Medicine","volume":"3 2","pages":"Article 100135"},"PeriodicalIF":0.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144168768","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Prognostic assessment of osteolytic lesions and mechanical properties of bones bearing breast cancer using neural network and finite element analysis☆ 基于神经网络和有限元分析的乳腺癌骨溶解病变和力学特性预后评估
Mechanobiology in Medicine Pub Date : 2025-06-01 Epub Date: 2025-03-30 DOI: 10.1016/j.mbm.2025.100130
Shubo Wang , Tiankuo Chu , Murtaza Wasi , Rosa M. Guerra , Xu Yuan , Liyun Wang
{"title":"Prognostic assessment of osteolytic lesions and mechanical properties of bones bearing breast cancer using neural network and finite element analysis☆","authors":"Shubo Wang ,&nbsp;Tiankuo Chu ,&nbsp;Murtaza Wasi ,&nbsp;Rosa M. Guerra ,&nbsp;Xu Yuan ,&nbsp;Liyun Wang","doi":"10.1016/j.mbm.2025.100130","DOIUrl":"10.1016/j.mbm.2025.100130","url":null,"abstract":"<div><div>The management of skeletal-related events (SREs), particularly the prevention of pathological fractures, is crucial for cancer patients. Current clinical assessment of fracture risk is mostly based on medical images, but incorporating sequential images in the assessment remains challenging. This study addressed this issue by leveraging a comprehensive dataset consisting of 260 longitudinal micro-computed tomography (μCT) scans acquired in normal and breast cancer bearing mice. A machine learning (ML) model based on a spatial–temporal neural network was built to forecast bone structures from previous μCT scans, which were found to have an overall similarity coefficient (Dice) of 0.814 with ground truths. Despite the predicted lesion volumes (18.5 ​% ​± ​15.3 ​%) being underestimated by ∼21 ​% than the ground truths’ (22.1 ​% ​± ​14.8 ​%), the time course of the lesion growth was better represented in the predicted images than the preceding scans (10.8 ​% ​± ​6.5 ​%). Under virtual biomechanical testing using finite element analysis (FEA), the predicted bone structures recapitulated the loading carrying behaviors of the ground truth structures with a positive correlation (y ​= ​0.863x) and a high coefficient of determination (R<sup>2</sup> ​= ​0.955). Interestingly, the compliances of the predicted and ground truth structures demonstrated nearly identical linear relationships with the lesion volumes. In summary, we have demonstrated that bone deterioration could be proficiently predicted using machine learning in our preclinical dataset, suggesting the importance of large longitudinal clinical imaging datasets in fracture risk assessment for cancer bone metastasis.</div></div>","PeriodicalId":100900,"journal":{"name":"Mechanobiology in Medicine","volume":"3 2","pages":"Article 100130"},"PeriodicalIF":0.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143807668","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Overstretch causes lipid accumulation in vascular smooth muscle cells dependent on NADPH oxidase 1 过度拉伸引起血管平滑肌细胞依赖于NADPH氧化酶1的脂质积累
Mechanobiology in Medicine Pub Date : 2025-06-01 Epub Date: 2025-03-26 DOI: 10.1016/j.mbm.2025.100129
Jiazhen Zhang , Qinfen Li , Suoqi Ding , Wei Xu , Jilei Su , Jingang Cui , Yongsheng Ding
{"title":"Overstretch causes lipid accumulation in vascular smooth muscle cells dependent on NADPH oxidase 1","authors":"Jiazhen Zhang ,&nbsp;Qinfen Li ,&nbsp;Suoqi Ding ,&nbsp;Wei Xu ,&nbsp;Jilei Su ,&nbsp;Jingang Cui ,&nbsp;Yongsheng Ding","doi":"10.1016/j.mbm.2025.100129","DOIUrl":"10.1016/j.mbm.2025.100129","url":null,"abstract":"<div><div>At the bend and bifurcation of arteries prone to atherosclerosis, pulsatile blood retention may cause overstretch on the tube wall. It has been reported that more than half of the foam cells found in atherosclerotic plaques are derived from vascular smooth muscle cells (VSMCs), but the mechanism is not adequately understood. In this work, we used a microfluidic device to apply a cyclic stretch (15 ​% and 0.05 ​Hz) on the VSMC for 24 ​h. The stretch caused a significant increase in the intracellular lipid accumulation, accompanying with the increased NOX1 and CD36 protein expression. On the other hand, inhibition of NOX1 activity, elimination of reactive oxygen species (ROS), or knockdown of NOX1 expression could significantly inhibit intracellular lipid accumulation. In addition, the NOX1 upregulation caused by 15 ​% stretch was related to the JAK/STAT signaling pathway. Our results reveal a novel mechanism of VSMC foam cell formation caused by the upregulation of NOX1.</div></div>","PeriodicalId":100900,"journal":{"name":"Mechanobiology in Medicine","volume":"3 2","pages":"Article 100129"},"PeriodicalIF":0.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143767683","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Multidimensional excavation of the current status and trends of mechanobiology in cardiovascular homeostasis and remodeling within 20 years 近20年来心血管稳态与重构的力学生物学研究现状与趋势的多维挖掘
Mechanobiology in Medicine Pub Date : 2025-06-01 Epub Date: 2025-03-19 DOI: 10.1016/j.mbm.2025.100127
Wei Liao , Yuxi Huang , Xiangxiu Wang , Ziqiu Hu , Chuanrong Zhao , Guixue Wang
{"title":"Multidimensional excavation of the current status and trends of mechanobiology in cardiovascular homeostasis and remodeling within 20 years","authors":"Wei Liao ,&nbsp;Yuxi Huang ,&nbsp;Xiangxiu Wang ,&nbsp;Ziqiu Hu ,&nbsp;Chuanrong Zhao ,&nbsp;Guixue Wang","doi":"10.1016/j.mbm.2025.100127","DOIUrl":"10.1016/j.mbm.2025.100127","url":null,"abstract":"<div><div>Mechanobiology is essential for cardiovascular structure and function and regulates the normal physiological and pathological processes of the cardiovascular system. Cells in the cardiovascular system are extremely sensitive to their mechanical environment, and once mechanical stimulation is abnormal, the homeostasis mechanism is damaged or lost, leading to the occurrence of pathological remodeling diseases. In the past 20 years, many articles concerning the mechanobiology of cardiovascular homeostasis and remodeling have been published. To better understand the current development status, research hotspots and future development trends in the field, this paper uses CiteSpace software for bibliometric analysis, quantifies and visualizes the articles published in this field in the past 20 years, and reviews the research hotspots and emerging trends. The regulatory effects of mechanical stimulation on the biological behavior of endothelial cells, smooth muscle cells and the extracellular matrix, as well as the mechanical-related remodeling mechanism in heart failure, have always been research hotspots in this field. This paper reviews the research advances of these research hotspots in detail. This paper also introduces the research status of emerging hotspots, such as those related to cardiac fibrosis, homeostasis, mechanosensitive transcription factors and mechanosensitive ion channels. We hope to provide a systematic framework and new ideas for follow-up research on mechanobiology in the field of cardiovascular homeostasis and remodeling and promote the discovery of more therapeutic targets and novel markers of mechanobiology in the cardiovascular system.</div></div>","PeriodicalId":100900,"journal":{"name":"Mechanobiology in Medicine","volume":"3 2","pages":"Article 100127"},"PeriodicalIF":0.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143714878","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Beyond biochemical patterning: How mechanical bistability governs robust organoid morphogenesis 超越生化模式:机械双稳定性如何控制强大的类器官形态发生
Mechanobiology in Medicine Pub Date : 2025-06-01 Epub Date: 2025-05-20 DOI: 10.1016/j.mbm.2025.100134
Qigan Gao, Yuehua Yang, Haoxiang Yang, Hongyuan Jiang
{"title":"Beyond biochemical patterning: How mechanical bistability governs robust organoid morphogenesis","authors":"Qigan Gao,&nbsp;Yuehua Yang,&nbsp;Haoxiang Yang,&nbsp;Hongyuan Jiang","doi":"10.1016/j.mbm.2025.100134","DOIUrl":"10.1016/j.mbm.2025.100134","url":null,"abstract":"<div><div>Understanding the regulatory mechanisms of intestinal organoid morphogenesis remains a fundamental challenge in organoid biology. Emerging evidence highlights mechanical bistability as a critical regulator, mediated by dynamic lumen-actomyosin feedback. The recently developed 3D vertex model demonstrates that crypt curvature modulates actomyosin localization via mechanosensitive pathways, creating two stable morphological states—bulged or budded—depending on mechanical history. This model advances beyond static vertex models by incorporating epithelial thickness variations and lumen pressure effects, explaining previously unresolved phenomena like irreversible crypt budding and snap-through transitions. The findings establish a new framework for understanding mechanical decision-making in epithelial tissues, with implications for organoid engineering and developmental biology.</div></div>","PeriodicalId":100900,"journal":{"name":"Mechanobiology in Medicine","volume":"3 2","pages":"Article 100134"},"PeriodicalIF":0.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144184941","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Gut microbiota-derived butyrate enhances exercise-induced bone mineral density in humans 肠道微生物来源的丁酸盐增强人体运动诱导的骨密度
Mechanobiology in Medicine Pub Date : 2025-06-01 Epub Date: 2025-03-05 DOI: 10.1016/j.mbm.2025.100124
Xiangya Dou , Pengyu Fu , Yuting Zhang , Yiwen Zhang , Kaiting Ning , Baoqiang Yang , Xuezhou Yang , Yinbo Niu , Dong-En Wang , Huiyun Xu
{"title":"Gut microbiota-derived butyrate enhances exercise-induced bone mineral density in humans","authors":"Xiangya Dou ,&nbsp;Pengyu Fu ,&nbsp;Yuting Zhang ,&nbsp;Yiwen Zhang ,&nbsp;Kaiting Ning ,&nbsp;Baoqiang Yang ,&nbsp;Xuezhou Yang ,&nbsp;Yinbo Niu ,&nbsp;Dong-En Wang ,&nbsp;Huiyun Xu","doi":"10.1016/j.mbm.2025.100124","DOIUrl":"10.1016/j.mbm.2025.100124","url":null,"abstract":"<div><div>Bone Mineral Density (BMD) is one of the primary markers of bone health. Exercise provides constant mechanical stress to bone, which in turn increases BMD. Gut-bone axis is considered to play an important role in the regulation of exercise on bone. Also, the metabolites of gut microbiota (GM), especially short-chain fatty acids (SCFAs), are thought to be involved in the progress. In this study, by analyzing serum and GM from humans with low and high BMD, we found that exercise indeed enhanced BMD, and butyrate secreted from GM was involved in the regulation.</div></div>","PeriodicalId":100900,"journal":{"name":"Mechanobiology in Medicine","volume":"3 2","pages":"Article 100124"},"PeriodicalIF":0.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143619478","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Tropomodulin1 regulates the biomechanical changes in macrophages induced by matrix stiffness Tropomodulin1调节基质刚度诱导巨噬细胞的生物力学变化
Mechanobiology in Medicine Pub Date : 2025-06-01 Epub Date: 2025-02-20 DOI: 10.1016/j.mbm.2025.100117
Yajun Meng , Amannisa Tuersuntuoheti , Siyu Jiang , Jiayi Xie , Zejun Yue , Dingwen Xu , Xueyu Geng , Xiang Lian , Lide Xie , Lanping Amy Sung , Xifu Wang , Jing Zhou , Weijuan Yao
{"title":"Tropomodulin1 regulates the biomechanical changes in macrophages induced by matrix stiffness","authors":"Yajun Meng ,&nbsp;Amannisa Tuersuntuoheti ,&nbsp;Siyu Jiang ,&nbsp;Jiayi Xie ,&nbsp;Zejun Yue ,&nbsp;Dingwen Xu ,&nbsp;Xueyu Geng ,&nbsp;Xiang Lian ,&nbsp;Lide Xie ,&nbsp;Lanping Amy Sung ,&nbsp;Xifu Wang ,&nbsp;Jing Zhou ,&nbsp;Weijuan Yao","doi":"10.1016/j.mbm.2025.100117","DOIUrl":"10.1016/j.mbm.2025.100117","url":null,"abstract":"<div><div>The monocyte/macrophage infiltration plays critical roles in the development of atherosclerosis. Arterial stiffness is a cholesterol-independent risk factor for cardiovascular events. The regulation of arterial stiffness on biomechanics of macrophages and its underlying mechanism remains unclear. We prepared polyacrylamide gels with low and high stiffness that corresponded to healthy and diseased blood vessels, respectively. We found that macrophages cultured on stiff matrix had increased rigidity and migration ability compared to those on soft matrix. An actin capping protein, tropomodulin1 (Tmod1) was upregulated in macrophages by stiff matrix and in arteries with high stiffness. Further analyses showed that deficiency of Tmod1 in macrophages completely or partially prevented the changes in actin polymerization, cell adhesion and cell spreading induced by stiff matrix. Overexpression of Tmod1 in macrophages enhanced actin polymerization, cell adhesion and spreading on stiff matrix. Tmod1 was involved in the regulation of vinculin expression and formation of focal adhesion in macrophages on stiff matrix. Finally, the deficiency of Tmod1 in macrophages retarded the formation of atherosclerotic plaques in blood vessels with high matrix stiffness. The results suggest that Tmod1 was a key regulator in macrophage rigidity and migration on stiff substrate. The present work will help us to understand the biomechanical mechanisms for the development of atherosclerosis.</div></div>","PeriodicalId":100900,"journal":{"name":"Mechanobiology in Medicine","volume":"3 2","pages":"Article 100117"},"PeriodicalIF":0.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143519903","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
The underlying difference of metastatic and non-metastatic breast cancer cells in configuring type I collagen fibres to promote migration by cell mechanics 转移性和非转移性乳腺癌细胞在配置I型胶原纤维通过细胞力学促进迁移方面的潜在差异
Mechanobiology in Medicine Pub Date : 2025-06-01 Epub Date: 2025-01-31 DOI: 10.1016/j.mbm.2025.100113
Mingxing Ouyang , Weihui Chen , Ting Zhou , Hongjie Liu , Lei Liu , Bing Bu , Linhong Deng
{"title":"The underlying difference of metastatic and non-metastatic breast cancer cells in configuring type I collagen fibres to promote migration by cell mechanics","authors":"Mingxing Ouyang ,&nbsp;Weihui Chen ,&nbsp;Ting Zhou ,&nbsp;Hongjie Liu ,&nbsp;Lei Liu ,&nbsp;Bing Bu ,&nbsp;Linhong Deng","doi":"10.1016/j.mbm.2025.100113","DOIUrl":"10.1016/j.mbm.2025.100113","url":null,"abstract":"<div><div>The progression of tumors is heavily influenced by mechanical properties of their microenvironment. In this work, we applied micropatterned models with varying distances and shapes to investigate the differences between metastatic MDA-MB-231 and non-metastatic MCF-7 breast cancer cells in reconfiguring extracellular matrix to promote cell migration induced by cell mechanics. Both cancer cells were able to rearrange type I collagen (COL) to form fibre threads, in which MDA-MB-231 consistently migrated more rapidly than MCF-7, ranging from geometrical square arrays with different spacings to complex polygonal models. MDA-MB-231 displayed higher capability of reorganizing fibre bundles at longer distance (800 ​μm). Further looking for differences in cell molecular mechanisms, siRNA knockdown inhibiting either integrin β1 or Piezo1 decreased fibre assembly and reduced the difference in COL remodeling and migration between two cancer cells. MDA-MB-231 showed inhibited migration with integrin knockdown, whereas scattering migration with Piezo1 knockdown, indicating cells losing directional mechanosensation. After inhibiting junctional E-cadherin with siRNA, MCF-7 cells migrated faster, resulting in reduced difference in comparison to MDA-MB-231 that didn't express E-cadherin. In summary, this work has explored the biomechanical differences between metastatic and non-metastatic breast cancer cells regarding COL fibre matrix remodeling and cell movements. The significant differences in E-cadherin expression in the two breast cancer cells had an effect on cell migrations. The results of this study provide research approaches for evaluating therapeutic effort on breast cancer.</div></div>","PeriodicalId":100900,"journal":{"name":"Mechanobiology in Medicine","volume":"3 2","pages":"Article 100113"},"PeriodicalIF":0.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143510220","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Mechanotransductive N-cadherin binding induces differentiation in human neural stem cells 机械传导性 N-粘连蛋白结合诱导人类神经干细胞分化
Mechanobiology in Medicine Pub Date : 2025-03-01 Epub Date: 2024-10-16 DOI: 10.1016/j.mbm.2024.100099
McKay Cavanaugh , Rebecca Kuntz Willits
{"title":"Mechanotransductive N-cadherin binding induces differentiation in human neural stem cells","authors":"McKay Cavanaugh ,&nbsp;Rebecca Kuntz Willits","doi":"10.1016/j.mbm.2024.100099","DOIUrl":"10.1016/j.mbm.2024.100099","url":null,"abstract":"<div><div>The neural stem cell niche is a complex microenvironment that includes cellular factors, secreted factors, and physical factors that impact stem cell behavior and development. Cellular interactions through cadherins, cell–cell binding proteins, have implications in embryonic development and mesenchymal stem cell differentiation. However, little is known about the influence of cadherins within the neural stem cell microenvironment and their effect on human stem cell maintenance and differentiation. Therefore, the purpose of this study was to develop synthetic substrates to examine the effect of cadherin mechanotransduction on human neural stem cells. Glass substrates were fabricated using silane, protein A, and recombinant N-cadherin; we used these substrates to examine the effect of N-cadherin binding on neural stem cell proliferation, cytoskeletal structure and morphology, Yes-associated protein-1 (YAP) translocation, and differentiation. Bound exogenous N-cadherin induced concentration-dependent increases in adherens junction formation, YAP translocation, and early expression of neurogenic differentiation markers. Strong F-actin ring structures were initiated by homophilic N-cadherin binding, eliciting neuronal differentiation of cells within 96 ​h without added soluble differentiation factors. Our findings show that active N-cadherin binding plays an important role for differentiation of human iPS-derived neural stem cells towards neurons, providing a new tool to differentiate cells <em>in vitro</em>.</div></div>","PeriodicalId":100900,"journal":{"name":"Mechanobiology in Medicine","volume":"3 1","pages":"Article 100099"},"PeriodicalIF":0.0,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142534812","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Toward a clear relationship between mechanical signals and bone adaptation 研究机械信号与骨适应之间的关系
Mechanobiology in Medicine Pub Date : 2025-03-01 Epub Date: 2025-02-01 DOI: 10.1016/j.mbm.2025.100115
Chenlu Wang, Ruisen Fu, Haisheng Yang
{"title":"Toward a clear relationship between mechanical signals and bone adaptation","authors":"Chenlu Wang,&nbsp;Ruisen Fu,&nbsp;Haisheng Yang","doi":"10.1016/j.mbm.2025.100115","DOIUrl":"10.1016/j.mbm.2025.100115","url":null,"abstract":"<div><div>Bone adapts according to the mechanical environment, and this adaptation can be visualized by altering its shape, size, and microarchitecture. Bone adaptation was recognized more than a century ago, with a description presented in <em>The Law of Bone Remodeling</em>. Furthermore, the conceptual model of “<em>The Mechanostat</em>” provides a quantitative relationship between the magnitude of bone tissue deformation (strain) and bone adaptive responses. However, upon maintaining a constant strain magnitude, various bone responses were observed experimentally under different loading parameters (e.g., frequency, rate, number of load cycles, rest insertion, and waveform). Nevertheless, the precise relationship between mechanical signals and bone adaptation remains unclear. Accordingly, we reviewed <em>in vivo</em> loading studies to determine the quantitative relationships between various mechanical signals and bone adaptive responses in various animal loading models. Additionally, we explored how these relationships are influenced by pathophysiological factors, such as age, sex, and estrogen deficiency. Moreover, mechanistic studies that consider cellular mechanical microenvironments to explain these quantitative relationships are discussed. A general formula that considers the bone adaptive response as a function of different loading parameters was proposed. This review may enhance our understanding of bone adaptation and offer guidance for clinicians to develop effective mechanotherapies to prevent bone loss.</div></div>","PeriodicalId":100900,"journal":{"name":"Mechanobiology in Medicine","volume":"3 1","pages":"Article 100115"},"PeriodicalIF":0.0,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143387379","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
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