Pub Date : 2025-03-26DOI: 10.1016/j.mbm.2025.100129
Jiazhen Zhang , Qinfen Li , Suoqi Ding , Wei Xu , Jilei Su , Jingang Cui , Yongsheng Ding
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.
{"title":"Overstretch causes lipid accumulation in vascular smooth muscle cells dependent on NADPH oxidase 1","authors":"Jiazhen Zhang , Qinfen Li , Suoqi Ding , Wei Xu , Jilei Su , Jingang Cui , 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":"2025-03-26","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}
Pub Date : 2025-03-19DOI: 10.1016/j.mbm.2025.100127
Wei Liao , Yuxi Huang , Xiangxiu Wang , Ziqiu Hu , Chuanrong Zhao , Guixue Wang
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.
{"title":"Multidimensional excavation of the current status and trends of mechanobiology in cardiovascular homeostasis and remodeling within 20 years","authors":"Wei Liao , Yuxi Huang , Xiangxiu Wang , Ziqiu Hu , Chuanrong Zhao , 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":"2025-03-19","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}
Pub Date : 2025-03-13DOI: 10.1016/j.mbm.2025.100128
Bingtong Yan , Minmin Lin , Yang Liu , Jiawei Li , Linjing Peng , Yifei Yao , Guangheng Li , Chao Liu
Meniscus horizontal tear is a common injury that mostly occurs in middle-aged and elderly people, and the effect of repair surgery directly affects the functional recovery of the knee joint and prevention of degenerative joint diseases. However, the stress concentration in a horizontal tear is not well understood. The primary objective of this study was to examine the reparative mechanisms involved in addressing horizontal tears of the meniscus and to elucidate the alterations in mechanical behavior throughout the subsequent postoperative healing stages. Based on clinical MRI scan data of normal human knee joint, an accurate three-dimensional finite element model of the knee joint was established to simulate the meniscus at different states: including complete, horizontal torn, repaired and at different degrees of healing. An animal model was established to conduct in vitro loading experiments to assist in validating the model. Static standing simulation revealed the phenomenon of stress concentration in the area of horizontal tears. Knee flexion simulations identified the risk of tear propagation at the endpoints of the horizontal tear. Following suture repair and progressive healing, stress concentration was observed at the site of sutures, while the stress levels decreased at the endpoints of the horizontal tear. As healing progressed, the mechanical function of the meniscus gradually recovered. During progressive healing, the changing trends can provide a reference for patients' postoperative recovery activities. This finding has important implications for guiding clinical treatment strategies and rehabilitation plans for meniscal tears.
{"title":"Biomechanics of horizontal meniscus tear and healing during knee flexion: Finite element analysis","authors":"Bingtong Yan , Minmin Lin , Yang Liu , Jiawei Li , Linjing Peng , Yifei Yao , Guangheng Li , Chao Liu","doi":"10.1016/j.mbm.2025.100128","DOIUrl":"10.1016/j.mbm.2025.100128","url":null,"abstract":"<div><div>Meniscus horizontal tear is a common injury that mostly occurs in middle-aged and elderly people, and the effect of repair surgery directly affects the functional recovery of the knee joint and prevention of degenerative joint diseases. However, the stress concentration in a horizontal tear is not well understood. The primary objective of this study was to examine the reparative mechanisms involved in addressing horizontal tears of the meniscus and to elucidate the alterations in mechanical behavior throughout the subsequent postoperative healing stages. Based on clinical MRI scan data of normal human knee joint, an accurate three-dimensional finite element model of the knee joint was established to simulate the meniscus at different states: including complete, horizontal torn, repaired and at different degrees of healing. An animal model was established to conduct in vitro loading experiments to assist in validating the model. Static standing simulation revealed the phenomenon of stress concentration in the area of horizontal tears. Knee flexion simulations identified the risk of tear propagation at the endpoints of the horizontal tear. Following suture repair and progressive healing, stress concentration was observed at the site of sutures, while the stress levels decreased at the endpoints of the horizontal tear. As healing progressed, the mechanical function of the meniscus gradually recovered. During progressive healing, the changing trends can provide a reference for patients' postoperative recovery activities. This finding has important implications for guiding clinical treatment strategies and rehabilitation plans for meniscal tears.</div></div>","PeriodicalId":100900,"journal":{"name":"Mechanobiology in Medicine","volume":"3 2","pages":"Article 100128"},"PeriodicalIF":0.0,"publicationDate":"2025-03-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143680447","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}
Pub Date : 2025-03-12DOI: 10.1016/j.mbm.2025.100125
Shaotian Fu , Yahong Lu , Wenkun Sun , Wugui Chen , Chengshou Lin , An Qin
Bone is an organ capable of perceiving external mechanical stress in real time and responding dynamically via mechanosensing proteins such as Piezo1 and YAP/TAZ. Upon sensing the mechano-signals, cells within the bone matrix collaborate to coordinate bone formation and resorption, while bone marrow cells are also stimulated and mobilized. High-load exercise stimulates osteoblast differentiation and bone formation. However, the mechanism through which the low-load exercises affect bone homeostasis is still unclear. In this work, we established a long-term swimming training model to unload the mechanical stress in mice. Throughout the training model, we observed a significant loss in trabecular bone mass, as evidenced by microCT scanning and histological staining. Single-cell sequencing of the tibial bone marrow tissue revealed a significant increase in the percentage of bone marrow neutrophils, along with alterations in Integrins and the ERK1/2 signaling pathway. Notably, the changes in both Integrins and the ERK1/2 signaling pathway in macrophages were more pronounced than in other cell types, which suggests a mechanical adaptive response in these cells. Moreover, the involvement of Integrins is also critical for the crosstalk between monocyte precusors and macrophages during swimming. Together, this study provides a resource of the alterations of bone marrow cell gene expression profile after swimming and highlights the importance of Integrins and the ERK1/2 signaling pathway in the bone marrow microenvironment after swimming.
{"title":"Swimming induces bone loss via regulating mechanical sensing pathways in bone marrow","authors":"Shaotian Fu , Yahong Lu , Wenkun Sun , Wugui Chen , Chengshou Lin , An Qin","doi":"10.1016/j.mbm.2025.100125","DOIUrl":"10.1016/j.mbm.2025.100125","url":null,"abstract":"<div><div>Bone is an organ capable of perceiving external mechanical stress in real time and responding dynamically via mechanosensing proteins such as Piezo1 and YAP/TAZ. Upon sensing the mechano-signals, cells within the bone matrix collaborate to coordinate bone formation and resorption, while bone marrow cells are also stimulated and mobilized. High-load exercise stimulates osteoblast differentiation and bone formation. However, the mechanism through which the low-load exercises affect bone homeostasis is still unclear. In this work, we established a long-term swimming training model to unload the mechanical stress in mice. Throughout the training model, we observed a significant loss in trabecular bone mass, as evidenced by microCT scanning and histological staining. Single-cell sequencing of the tibial bone marrow tissue revealed a significant increase in the percentage of bone marrow neutrophils, along with alterations in Integrins and the ERK1/2 signaling pathway. Notably, the changes in both Integrins and the ERK1/2 signaling pathway in macrophages were more pronounced than in other cell types, which suggests a mechanical adaptive response in these cells. Moreover, the involvement of Integrins is also critical for the crosstalk between monocyte precusors and macrophages during swimming. Together, this study provides a resource of the alterations of bone marrow cell gene expression profile after swimming and highlights the importance of Integrins and the ERK1/2 signaling pathway in the bone marrow microenvironment after swimming.</div></div>","PeriodicalId":100900,"journal":{"name":"Mechanobiology in Medicine","volume":"3 2","pages":"Article 100125"},"PeriodicalIF":0.0,"publicationDate":"2025-03-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143636634","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}
Pub Date : 2025-03-11DOI: 10.1016/j.mbm.2025.100126
Ryosuke Yokosawa , Rachel A. Mazur , Kelsey A. Wilson , Jacob H. Lee , Noah W. Showalter , Kyle J. Lampe , Pamela J. VandeVord
Traumatic brain injury (TBI) leads to neuroinflammation and is associated with chronic neurodegeneration. Many TBI studies aim to understand further the mechanism by which cells in the brain respond to the mechanical forces associated with TBI. In particular, mild TBI is the most common level of injury among TBI patients, and the reactivity of glial cells is a key mechanism in understanding mild TBI. However, there is a lack of studies focusing on oligodendrocyte precursor cells (OPCs). OPCs respond to the injury by migration, proliferation, and differentiation into oligodendrocytes (OL) to assist in post-injury repair. Given their ability to proliferate and differentiate, OPCs are a promising therapeutic target for OL regeneration. Despite their important role in maintaining normal neuronal functions, the response of OPCs to mechanical insult remains poorly understood. Thus, this study aims to elucidate the cellular responses of OPCs using a brain-tissue mimicking in vitro 3D hydrogel platform to identify key signaling pathways driving their response. In this study, we applied a high-rate pressure wave to OPCs to induce mild TBI and assess subsequent cellular and molecular responses by quantifying cell growth, metabolic activity, and gene and protein expression. Although the high-rate mechanical insult did not significantly impact cell survival, it induced transcriptomic and proteomic changes in molecular targets related to OPC proliferation and maturation, including PDGFRA, GALC, CTNNB1, and HSP90AB. These dysregulations and altered molecular profiles provide valuable insights into the OPC injury response and may serve as potential therapeutic targets for treating neurodegeneration.
{"title":"High-rate mechano-stimulation alters proliferation- and maturation-related signaling of oligodendrocyte precursor cells in a 3D hydrogel","authors":"Ryosuke Yokosawa , Rachel A. Mazur , Kelsey A. Wilson , Jacob H. Lee , Noah W. Showalter , Kyle J. Lampe , Pamela J. VandeVord","doi":"10.1016/j.mbm.2025.100126","DOIUrl":"10.1016/j.mbm.2025.100126","url":null,"abstract":"<div><div>Traumatic brain injury (TBI) leads to neuroinflammation and is associated with chronic neurodegeneration. Many TBI studies aim to understand further the mechanism by which cells in the brain respond to the mechanical forces associated with TBI. In particular, mild TBI is the most common level of injury among TBI patients, and the reactivity of glial cells is a key mechanism in understanding mild TBI. However, there is a lack of studies focusing on oligodendrocyte precursor cells (OPCs). OPCs respond to the injury by migration, proliferation, and differentiation into oligodendrocytes (OL) to assist in post-injury repair. Given their ability to proliferate and differentiate, OPCs are a promising therapeutic target for OL regeneration. Despite their important role in maintaining normal neuronal functions, the response of OPCs to mechanical insult remains poorly understood. Thus, this study aims to elucidate the cellular responses of OPCs using a brain-tissue mimicking <em>in vitro</em> 3D hydrogel platform to identify key signaling pathways driving their response. In this study, we applied a high-rate pressure wave to OPCs to induce mild TBI and assess subsequent cellular and molecular responses by quantifying cell growth, metabolic activity, and gene and protein expression. Although the high-rate mechanical insult did not significantly impact cell survival, it induced transcriptomic and proteomic changes in molecular targets related to OPC proliferation and maturation, including <em>PDGFRA</em>, <em>GALC</em>, CTNNB1, and HSP90AB. These dysregulations and altered molecular profiles provide valuable insights into the OPC injury response and may serve as potential therapeutic targets for treating neurodegeneration.</div></div>","PeriodicalId":100900,"journal":{"name":"Mechanobiology in Medicine","volume":"3 3","pages":"Article 100126"},"PeriodicalIF":0.0,"publicationDate":"2025-03-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144169323","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}
Pub Date : 2025-03-05DOI: 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
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.
{"title":"Gut microbiota-derived butyrate enhances exercise-induced bone mineral density in humans","authors":"Xiangya Dou , Pengyu Fu , Yuting Zhang , Yiwen Zhang , Kaiting Ning , Baoqiang Yang , Xuezhou Yang , Yinbo Niu , Dong-En Wang , 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":"2025-03-05","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}
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.
{"title":"Tropomodulin1 regulates the biomechanical changes in macrophages induced by matrix stiffness","authors":"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","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":"2025-02-20","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}
Pub Date : 2025-02-19DOI: 10.1016/j.mbm.2025.100116
Yi-Xian Qin
Ultrasound imaging has been widely used in clinical diagnoses, such as B-mode and M-mode ultrasound imaging for cardiovascular, abdomen, OB-Gyn, and other soft tissue and organs in clinical diagnoses. Ultrasound imaging has traditionally been limited in its application to bone because of the high acoustic impedance and density of trabecular and cortical bone structure and density alterations, high wave reflection, absorption, scattering, and low penetration, which result in significant reflection and attenuation of ultrasonic energy in such mineral tissues. Recent advancements in quantitative ultrasound technology have opened new possibilities for noninvasive characteristics of bone quality through transmitted or backscattered signals, offering a radiation-free alternative to traditional imaging modalities like dual-energy X-ray absorptiometry (DEX), X-rays, and CT scans. In addition, low-intensity ultrasound (LIUS) has been studied and applied to promote bone regeneration and fracture healing through induced mechanotransduction in tissue and cells. The field of bone ultrasound encompasses fundamental research on the interaction of elastic waves with cortical and trabecular bone microstructures, the development of innovative imaging methodologies and medical applications such as bone health assessment for osteoporosis diagnosis, therapeutic use of LIUS, and phase aberration correction inside the skull. This work has highlighted recent developments and advancements in ultrasound diagnosis and therapeutics, induced cellular and molecular pathways, and future directions using ultrasound as a promising imaging tool and treatment method.
{"title":"Ultrasound imaging and regulated mechanotransduction for characteristics, regeneration, and therapeutics of bone","authors":"Yi-Xian Qin","doi":"10.1016/j.mbm.2025.100116","DOIUrl":"10.1016/j.mbm.2025.100116","url":null,"abstract":"<div><div>Ultrasound imaging has been widely used in clinical diagnoses, such as B-mode and M-mode ultrasound imaging for cardiovascular, abdomen, OB-Gyn, and other soft tissue and organs in clinical diagnoses. Ultrasound imaging has traditionally been limited in its application to bone because of the high acoustic impedance and density of trabecular and cortical bone structure and density alterations, high wave reflection, absorption, scattering, and low penetration, which result in significant reflection and attenuation of ultrasonic energy in such mineral tissues. Recent advancements in quantitative ultrasound technology have opened new possibilities for noninvasive characteristics of bone quality through transmitted or backscattered signals, offering a radiation-free alternative to traditional imaging modalities like dual-energy X-ray absorptiometry (DEX), X-rays, and CT scans. In addition, low-intensity ultrasound (LIUS) has been studied and applied to promote bone regeneration and fracture healing through induced mechanotransduction in tissue and cells. The field of bone ultrasound encompasses fundamental research on the interaction of elastic waves with cortical and trabecular bone microstructures, the development of innovative imaging methodologies and medical applications such as bone health assessment for osteoporosis diagnosis, therapeutic use of LIUS, and phase aberration correction inside the skull. This work has highlighted recent developments and advancements in ultrasound diagnosis and therapeutics, induced cellular and molecular pathways, and future directions using ultrasound as a promising imaging tool and treatment method.</div></div>","PeriodicalId":100900,"journal":{"name":"Mechanobiology in Medicine","volume":"3 1","pages":"Article 100116"},"PeriodicalIF":0.0,"publicationDate":"2025-02-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143480292","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}
Pub Date : 2025-02-01DOI: 10.1016/j.mbm.2025.100115
Chenlu Wang, Ruisen Fu, Haisheng Yang
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 The Law of Bone Remodeling. Furthermore, the conceptual model of “The Mechanostat” 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 in vivo 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.
{"title":"Toward a clear relationship between mechanical signals and bone adaptation","authors":"Chenlu Wang, Ruisen Fu, 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}
Pub Date : 2025-02-01DOI: 10.1016/j.mbm.2025.100114
Hanxiao Chen , Chengxiu Peng , Fei Fang , Yuhao Li , Xiaran Liu , Ying Hu , Guixue Wang , Xiaoheng Liu , Yang Shen
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.
{"title":"Angiogenesis within atherosclerotic plaques: Mechanical regulation, molecular mechanism and clinical diagnosis","authors":"Hanxiao Chen , Chengxiu Peng , Fei Fang , Yuhao Li , Xiaran Liu , Ying Hu , Guixue Wang , Xiaoheng Liu , 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}
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