Mechanobiology in Medicine最新文献

{"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":"2025-02-01","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}

{"title":"Angiogenesis within atherosclerotic plaques: Mechanical regulation, molecular mechanism and clinical diagnosis","authors":"Hanxiao Chen ,&nbsp;Chengxiu Peng ,&nbsp;Fei Fang ,&nbsp;Yuhao Li ,&nbsp;Xiaran Liu ,&nbsp;Ying Hu ,&nbsp;Guixue Wang ,&nbsp;Xiaoheng Liu ,&nbsp;Yang Shen","doi":"10.1016/j.mbm.2025.100114","DOIUrl":"10.1016/j.mbm.2025.100114","url":null,"abstract":"<div><div>Atherosclerosis (AS) is a disease characterized by focal cholesterol accumulation and insoluble inflammation in arterial intima, leading to the formation of an atherosclerotic plaque consisting of lipids, cells, and fibrous matrix. The presence of plaque can restrict or obstruct blood flow, resulting in arterial stenosis and local mechanical microenvironment changes including flow shear stress, vascular matrix stiffness, and plaque structural stress. Neovascularization within the atherosclerotic plaque plays a crucial role in both plaque growth and destabilization, potentially leading to plaque rupture and fatal embolism. However, the exact interactions between neovessels and plaque remain unclear. In this review, we provide a comprehensive analysis of the origin of intraplaque neovessels, the contributing factors, underlying molecular mechanisms, and associated signaling pathways. We specifically emphasize the role of mechanical factors contributing to angiogenesis in atherosclerotic plaques. Additionally, we summarize the imaging techniques and therapeutic strategies for intraplaque neovessels to enhance our understanding of this field.</div></div>","PeriodicalId":100900,"journal":{"name":"Mechanobiology in Medicine","volume":"3 1","pages":"Article 100114"},"PeriodicalIF":0.0,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143428126","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}

{"title":"Mechanotransduction and inflammation: An updated comprehensive representation","authors":"Vennila Suriyagandhi ,&nbsp;Ying Ma ,&nbsp;Veronica Paparozzi ,&nbsp;Tiziana Guarnieri ,&nbsp;Biagio Di Pietro ,&nbsp;Giovanna Maria Dimitri ,&nbsp;Paolo Tieri ,&nbsp;Claudia Sala ,&nbsp;Darong Lai ,&nbsp;Christine Nardini","doi":"10.1016/j.mbm.2024.100112","DOIUrl":"10.1016/j.mbm.2024.100112","url":null,"abstract":"<div><div>Mechanotransduction is the process that enables the conversion of mechanical cues into biochemical signaling. While all our cells are well known to be sensitive to such stimuli, the details of the systemic interaction between mechanical input and inflammation are not well integrated. Often, indeed, they are considered and studied in relatively compartmentalized areas, and we therefore argue here that to understand the relationship of mechanical stimuli with inflammation – with a high translational potential - it is crucial to offer and analyze a unified view of mechanotransduction. We therefore present here pathway representation, recollected with the standard systems biology markup language (SBML) and explored with network biology approaches, offering RAC1 as an exemplar and emerging molecule with potential for medical translation.</div></div>","PeriodicalId":100900,"journal":{"name":"Mechanobiology in Medicine","volume":"3 1","pages":"Article 100112"},"PeriodicalIF":0.0,"publicationDate":"2024-12-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143165421","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}

{"title":"Matrix stiffness and viscoelasticity influence human mesenchymal stem cell immunomodulation","authors":"Sara J. Olsen ,&nbsp;Rose E. Leader ,&nbsp;Abigail L. Mortimer ,&nbsp;Bethany Almeida","doi":"10.1016/j.mbm.2024.100111","DOIUrl":"10.1016/j.mbm.2024.100111","url":null,"abstract":"<div><div>Human mesenchymal stem cells (hMSCs) have immense wound healing potential due to their immunomodulatory behavior. To control this behavior and reduce heterogeneity, researchers look to biomaterials, as matrix stiffness and viscoelasticity have been shown to control hMSC immunomodulation. However, the understanding of the effects of these biophysical cues on hMSC immunomodulation remains limited; a broad study investigating the potentially synergistic effects of matrix stiffness and viscoelasticity on hMSC immunomodulation is needed in order to support future work developing biomaterials for hMSC wound healing applications. We developed polyacrylamide (PAAm) gels with varying matrix stiffnesses with or without a viscoelastic element and explored the effects of these on hMSC-matrix interactions and immunomodulatory cytokine expression in both a normal growth media and an immunomodulatory growth media mimetic of a chronic, non-healing wound. Expression of IL-10, VEGF, and PGE₂ were upregulated in immunomodulatory growth media over normal growth media, demonstrating the synergistic effects of biochemical signaling on hMSC immunomodulatory behavior. In addition, the addition of a viscoelastic element had both inhibitory and accentuating effects based on the cytokine and biochemical signaling in the cell culture media. Overall, this study provides a broad perspective on the immunomodulatory behavior of hMSCs due to stiffness and viscoelasticity.</div></div>","PeriodicalId":100900,"journal":{"name":"Mechanobiology in Medicine","volume":"3 1","pages":"Article 100111"},"PeriodicalIF":0.0,"publicationDate":"2024-12-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143165418","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}

{"title":"The first embryo, the origin of cancer and animal phylogeny. V. Cancer stem cells as the unifying biomechanical principle between embryology and oncology","authors":"Jaime Cofre","doi":"10.1016/j.mbm.2024.100110","DOIUrl":"10.1016/j.mbm.2024.100110","url":null,"abstract":"<div><div>The role of embryology in metazoan evolution is rooted deeply in the history of science. Viewing Neoplasia as an evolutionary engine provides a scientific basis for reexamining the disease cancer. Once the embryo is understood as a benign tumor with a pivotal role in the evolution of all animal forms, there will be an immediate paradigm shift in the search for cancer cure, potentially revealing insights that may be buried within the great developmental transitions of metazoans. This article discusses one of the unifying principles between embryology and oncology, namely cancer stem cells. Some considerations are also provided on the central role of physics and biomechanics in the assembly of the first embryo, which can be regarded as a differentiated benign tumor. Mechanical impregnation of the nucleus of a stem cell, culminating in a totipotent/multipotent cell, was a major event safeguarding the success of embryogenesis throughout evolution. Germ cells in the earliest ctenophore embryos underwent delayed differentiation, subsequent to the mechanical assembly of the embryo. Finally, a discussion is presented on the concept that cancer and embryogenesis (cancer and healthy stem cells) are two sides of the same coin, that is, of the same process. The only difference is that cancer stem cells reveal themselves in inappropriate contexts. Neoplasia is a free force, whereas cancer is a force contained by animal organization.</div></div>","PeriodicalId":100900,"journal":{"name":"Mechanobiology in Medicine","volume":"3 1","pages":"Article 100110"},"PeriodicalIF":0.0,"publicationDate":"2024-12-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143165420","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}

{"title":"Harnessing mechanobiology to enhance cell therapy","authors":"Peixiang Ma ,&nbsp;An Qin ,&nbsp;Tobias Winkler ,&nbsp;Jie Zhao","doi":"10.1016/j.mbm.2024.100102","DOIUrl":"10.1016/j.mbm.2024.100102","url":null,"abstract":"<div><div>Recent developments in cell therapy have revolutionized medical treatment. While various methods of stimulation have been explored, the role of mechanical force has often been overlooked. Although mechanical loading is not easily visible, it can actively reshape organisms, and abnormal mechanical loading can lead to injury and disease. By leveraging the mechanobiology of cells, we can equip them with synthetic mechanosensors that can redirect genetic circuits to express protective factors, such as antibodies and cytokines, according to the mechanical force signal. The advancement of artificial intelligence (AI) presents a fascinating opportunity to redesign more complex mechanoreceptors, allowing cells to respond to intricate stimuli. Additionally, genetic engineering tools like CRISPR-Cas9, base editing, and prime editing enable the creation of multiple gene circuits for cells to react to complex mechanical environments. Advanced mechanical loading techniques, such as focused ultrasound, deliver signals in a confined spatial and temporal manner. Therefore, harnessing mechanobiology in cells can develop more flexible, personalized, and precise cell therapies.</div></div>","PeriodicalId":100900,"journal":{"name":"Mechanobiology in Medicine","volume":"2 4","pages":"Article 100102"},"PeriodicalIF":0.0,"publicationDate":"2024-11-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142723640","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}

{"title":"miRNA in mechanobiology: The exploration needs to continue","authors":"Kai Huang,&nbsp;Yingxin Qi","doi":"10.1016/j.mbm.2024.100101","DOIUrl":"10.1016/j.mbm.2024.100101","url":null,"abstract":"<div><div>The 2024 Nobel Prize in Physiology or Medicine has once again sparked considerable interest in microRNA (miRNA). Recent advances have unveiled that miRNAs play critical roles in mediating the effects of mechanical stimuli on gene expression, cellular functions, tissue development, and disease progression. This perspective summarized the history of miRNA research and highlighted the promising research directions of miRNAs in the field of mechanobiology.</div></div>","PeriodicalId":100900,"journal":{"name":"Mechanobiology in Medicine","volume":"2 4","pages":"Article 100101"},"PeriodicalIF":0.0,"publicationDate":"2024-11-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142703966","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}

{"title":"Mechanobiological cues to bone cells during early metastasis drive later osteolysis: A computational mechanoregulation framework prediction","authors":"Anneke S.K. Verbruggen ,&nbsp;Elan C. McCarthy ,&nbsp;Roisin M. Dwyer ,&nbsp;Laoise M. McNamara","doi":"10.1016/j.mbm.2024.100100","DOIUrl":"10.1016/j.mbm.2024.100100","url":null,"abstract":"<div><div>Bone cells contribute to tumour metastasis by producing biochemical factors that stimulate tumour cell homing and proliferation, but also by resorbing bone matrix (osteolysis) that releases further stimulatory factors for tumour growth in a vicious cycle. Changes in the local mechanical environment of bone tissue occur during early metastasis, which might activate mechanobiological responses by resident bone cells (osteocytes) to activate resorption (osteoclasts) and thereby contribute to tumour invasion. The objective of this study is to investigate whether bone osteolysis is driven by early changes in the bone mechanical environment during metastasis by (a) implementing subject-specific FE models of metastatic femora to predict the mechanical environment within bone tissue during early metastasis (3-weeks after tumour inoculation) and then (b) applying mechanoregulation theory to predict bone tissue remodelling as a function of the evolving mechanical environment within bone tissue during breast cancer-bone metastasis. We implemented a global resorption rate derived from an experimental model, but the mechanoregulation algorithm predicted localised bone loss in the greater trochanter region, the same region where osteolysis was prevalent after three weeks of metastasis development in the animal model. Moreover, the mechanical environment evolved in a similar manner to that reported in separate subject-specific finite element models of these same animals by 6 weeks. Thus, we propose that early changes in the physical environment of bone tissue during metastasis may elicit mechanobiological cues for bone cells and activate later osteolytic bone destruction.</div></div>","PeriodicalId":100900,"journal":{"name":"Mechanobiology in Medicine","volume":"3 1","pages":"Article 100100"},"PeriodicalIF":0.0,"publicationDate":"2024-10-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143165419","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}

{"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":"2024-10-16","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}

{"title":"Relationship between bilateral symmetry of foot posture and lower limb musculoskeletal injuries among workers engaged in physically demanding occupations: A cross-sectional investigation","authors":"Chunhua Liao ,&nbsp;Jing Liu ,&nbsp;Shuanglong Hou ,&nbsp;Wendong Zhang ,&nbsp;Xin Zhao ,&nbsp;Zhipan Hou ,&nbsp;Honglei Quan ,&nbsp;Zhaohui Tian ,&nbsp;Rui Liu ,&nbsp;Yuting Zhao","doi":"10.1016/j.mbm.2024.100098","DOIUrl":"10.1016/j.mbm.2024.100098","url":null,"abstract":"<div><div>Even though the link between foot posture and lower-extremity injuries remains controversial, there has been little research focus on bilateral foot symmetry. This study evaluated the correlation between bilateral symmetry in foot posture and lower extremity musculoskeletal injuries among workers in physically intensive occupations. A total of 248 participants with physically demanding roles were enrolled. Historical data on lower-limb musculoskeletal injuries were obtained through a review of medical records, supplemented by results from on-site consultations. The foot arch index (AI) was quantitatively measured using a 3D laser foot scanner, and foot posture was evaluated using the foot posture index-6 (FPI-6). The participants were categorized into subgroups based on bilateral symmetry assessments of their feet. Logistic regression analyses were performed for statistical comparisons after adjusting for potential confounding factors. The results indicate that abnormalities in foot posture and arch, assessed using the FPI-6 and AI, were identified in 42.3 ​% and 47.2 ​% of participants, respectively, with 20.9 ​% and 16.5 ​% demonstrating bilateral asymmetry in these parameters. When comparing bilateral and unilateral foot protonation with bilaterally normal feet, the risk adjustments revealed differences of 2.274 (95 ​% CI: 1.094–4.729, <em>P</em> ​= ​0.028) and 2.751 (95 ​% CI: 1.222–6.191, <em>P</em> ​= ​0.015), respectively. Furthermore, the risk adjustment for age, BMI, smoking status, physical training years, training time, training frequency, warm-up before training, relaxation after training, MIS prevention, and treatment learning for unilateral flatfoot relative to bilateral normal feet was 3.197 (95 ​% CI:1.235–8.279, <em>P</em> ​= ​0.017). This study demonstrates that workers in physically demanding occupations who exhibit unilateral foot protonation or unilateral flatfoot are at an increased risk of lower-extremity musculoskeletal injuries.</div></div>","PeriodicalId":100900,"journal":{"name":"Mechanobiology in Medicine","volume":"3 1","pages":"Article 100098"},"PeriodicalIF":0.0,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142534805","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}