Xinman Chen , Chenyang Ji , Xi Liu , Ning Wang , Fuxiang Wei , Junwei Chen
{"title":"Three-dimensional traction technology and its application in mechanomedicine","authors":"Xinman Chen , Chenyang Ji , Xi Liu , Ning Wang , Fuxiang Wei , Junwei Chen","doi":"10.1016/j.mbm.2025.100131","DOIUrl":"10.1016/j.mbm.2025.100131","url":null,"abstract":"<div><div>Endogenous forces generated by living cells are essential for biological processes and physiological functions of cells and tissues. Over the last several decades, numerous methods for detecting traction forces have been developed. Here we review these methods and discuss their respective strengths and limitations. Being able to reliably quantify tractions in living cells and tissues are critical in understanding how forces drive and regulate cell and tissue functions in physiology and diseases.</div></div>","PeriodicalId":100900,"journal":{"name":"Mechanobiology in Medicine","volume":"3 3","pages":"Article 100131"},"PeriodicalIF":0.0,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143906111","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}
Yibo Feng , Bingchen Che , Yonggang Liu , Cangmin Zhang , Jiameng Niu , Jiangcun Yang , Guangyin Jing , Dan Sun , Xiaobo Gong , Ce Zhang
{"title":"Early diabetes screening via red blood cell mechanics using microfluidic chip integration","authors":"Yibo Feng , Bingchen Che , Yonggang Liu , Cangmin Zhang , Jiameng Niu , Jiangcun Yang , Guangyin Jing , Dan Sun , Xiaobo Gong , Ce Zhang","doi":"10.1016/j.mbm.2025.100136","DOIUrl":"10.1016/j.mbm.2025.100136","url":null,"abstract":"<div><div>Early diagnosis of diabetes is crucial, as diabetes, particularly type 2, can eventually lead to irreversible changes and complications. Conventional techniques, such as the Fasting Plasma Glucose (FPG) Test and Hemoglobin A1c (HbA1c) Test, measure blood glucose levels, which fluctuate over time and are insensitive to early stages. In this study, we focus on measuring the mechanical properties of red blood cells, as their irreversible changes can indicate early pathological impacts of diabetes. We developed a microfluidic chip with a symmetrical hyperbolic structure. By periodically altering the state of the valve membrane, we generate a reciprocating shear flow field that repeatedly acts on groups of RBCs. We then quantify the morphological parameters of the RBCs, establishing a correlation between the reciprocating shear flow field and the morphological changes of the cells. Using the developed microfluidic chip, we investigated the resistance of blood cells from 20 healthy volunteers to mechanical stimuli. The results indicated a significant correlation between the deformability of red blood cells and age, while no such correlation was found among individuals of the same gender. This study highlights the potential of utilizing the mechanical properties of red blood cells as an early diagnostic tool for diabetes. Furthermore, given the ease of integration of microfluidic chips, they present a promising high-throughput diagnostic solution for large-scale clinical screening.</div></div>","PeriodicalId":100900,"journal":{"name":"Mechanobiology in Medicine","volume":"3 3","pages":"Article 100136"},"PeriodicalIF":0.0,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144242828","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}
Ryosuke Yokosawa , Rachel A. Mazur , Kelsey A. Wilson , Jacob H. Lee , Noah W. Showalter , Kyle J. Lampe , Pamela J. VandeVord
{"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":"2025-09-01","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}
Kaiyang Wang , Shuhui Ren , Yunfang Jia , Xiaobing Yan , Lizhen Wang , Yubo Fan
{"title":"Neuromorphic chips for biomedical engineering","authors":"Kaiyang Wang , Shuhui Ren , Yunfang Jia , Xiaobing Yan , Lizhen Wang , Yubo Fan","doi":"10.1016/j.mbm.2025.100133","DOIUrl":"10.1016/j.mbm.2025.100133","url":null,"abstract":"<div><div>The modern medical field faces two critical challenges: the dramatic increase in data complexity and the explosive growth in data size. Especially in current research, medical diagnostic, and data processing devices relying on traditional computer architecture are increasingly showing limitations when faced with dynamic temporal and spatial processing requirements, as well as high-dimensional data processing tasks. Neuromorphic devices provide a new way for biomedical data processing due to their low energy consumption and high dynamic information processing capabilities. This paper aims to reveal the advantages of neuromorphic devices in biomedical applications. First, this review emphasizes the urgent need of biomedical engineering for diversify clinical diagnostic techniques. Secondly, the feasibility of the application in biomedical engineering is demonstrated by reviewing the historical development of neuromorphic devices from basic modeling to multimodal signal processing. In addition, this paper demonstrates the great potential of neuromorphic chips for application in the fields of biosensing technology, medical image processing and generation, rehabilitation medical engineering, and brain-computer interfaces. Finally, this review provides the pathways for constructing standardized experimental protocols using biocompatible technologies, personalized treatment strategies, and systematic clinical validation. In summary, neuromorphic devices will drive technological innovation in the biomedical field and make significant contributions to life health.</div></div>","PeriodicalId":100900,"journal":{"name":"Mechanobiology in Medicine","volume":"3 3","pages":"Article 100133"},"PeriodicalIF":0.0,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144169324","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}
{"title":"Mitochondria power the nucleus under pressure","authors":"Meng Yao , Yao Zong , Junjie Gao","doi":"10.1016/j.mbm.2025.100146","DOIUrl":"10.1016/j.mbm.2025.100146","url":null,"abstract":"<div><div>Mechanical confinement of cells, as occurs during processes like tumor cell invasion or immune cell trafficking, poses a pressure that can threaten nuclear integrity and cell viability. Recent findings illuminate a rapid adaptive mechanism by which cells under acute compressive stress rearrange their internal architecture to preserve nuclear functions. Upon confinement, mitochondria swiftly relocate to cluster around the nucleus (forming nuclear-associated mitochondria, NAM), entrapped by a web of endoplasmic reticulum (ER) and actin filaments. This proximity provides a localized surge of ATP within the nucleus, fueling energy-intensive nuclear processes, notably maintaining an open chromatin state and facilitating efficient DNA damage repair. This targeted energy delivery maintains nuclear chromatin accessibility, supports DNA repair mechanisms, and ensures sustained cell proliferation despite physical constraints. Here we provide a commentary on these findings, discussing the biological significance of mitochondria–nucleus repositioning, the role of nuclear ATP in safeguarding chromatin, and the broader implications for cellular fitness in development and disease.</div></div>","PeriodicalId":100900,"journal":{"name":"Mechanobiology in Medicine","volume":"3 3","pages":"Article 100146"},"PeriodicalIF":0.0,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144878563","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}
Timothy Hung , Kaitlyn S. Broz , Remy E. Walk , Simon Y. Tang
{"title":"The sex-specific effects of RAGE signaling and type 2 diabetes on mouse cortical bone mechanics, structure, and material properties","authors":"Timothy Hung , Kaitlyn S. Broz , Remy E. Walk , Simon Y. Tang","doi":"10.1016/j.mbm.2025.100132","DOIUrl":"10.1016/j.mbm.2025.100132","url":null,"abstract":"<div><div>Individuals with type 2 diabetes (T2D) are prone to fracture at numerous skeletal sites despite presenting with a higher bone mineral density (BMD). The accumulation of Advanced Glycation End-products (AGEs) in the bone tissues of patients with T2D could be contributing to this paradox of increased skeletal fragility with higher BMD. AGEs can also impair bone cell homeostasis via the receptor for AGEs (RAGE). To investigate the effects of diabetes, AGE accumulation, and RAGE signaling on mouse cortical bone, we utilized male and female leptin receptor-deficient (db/db) diabetic mice from three age groups ranging from 3 to 12 months of age, which were crossed with mice carrying constitutively active alleles for a RAGE nullifying point mutation (RAGE<sup>−/−</sup>). The morphological, mechanical and material outcomes of bone were measured using microCT, three-point bending, and AGE assays. We observed significant impairments dependent on age and sex to the bone matrix and whole-bone mechanical behavior due to diabetes, with some impairments alleviated by the deletion of RAGE. In older female diabetic mice, the removal of RAGE signaling prevented the deficits in bone mechanics, morphology, and tissue mineral density (TMD). Male diabetic mice without RAGE signaling exhibited improved material properties compared to wild type controls. The study demonstrated that bone impairments associated with T2D can be prevented with RAGE deletion, and T2D complications may be partially reversible with the therapeutic inhibition of RAGE signaling.</div></div>","PeriodicalId":100900,"journal":{"name":"Mechanobiology in Medicine","volume":"3 3","pages":"Article 100132"},"PeriodicalIF":0.0,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144169054","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}
Alanna Krug , Gabrielle Inserra , Rhonda Drewes , Amanda Krajnik , Joseph A. Brazzo III , Thomas Mousso , Su Chin Heo , Yongho Bae
{"title":"Three-dimensional spheroid models for cardiovascular biology and pathology","authors":"Alanna Krug , Gabrielle Inserra , Rhonda Drewes , Amanda Krajnik , Joseph A. Brazzo III , Thomas Mousso , Su Chin Heo , Yongho Bae","doi":"10.1016/j.mbm.2025.100144","DOIUrl":"10.1016/j.mbm.2025.100144","url":null,"abstract":"<div><div>Scaffold-free three-dimensional (3D) cellular spheroid cultures better replicate the <em>in vivo</em> cellular microenvironments of complex tissues than traditional two-dimensional (2D) cell cultures, as they promote more intricate cell-cell and cell-extracellular matrix (ECM) interactions. In the context of cardiovascular research, 3D spheroids have emerged as valuable models for studying angiogenesis, modeling the cardiac microenvironment, and advancing drug development and cardiac tissue repair. Given that cardiovascular disease remains the leading cause of morbidity worldwide, exploring 3D spheroids as <em>in vitro</em> models in cardiovascular research holds potential for advancing the field. Despite their promise, the experimental potential of 3D spheroids in cardiovascular disease and biology has yet to be realized. Therefore, this review discusses the advantages and limitations of 3D spheroid models for studying angiogenesis and cardiovascular pathobiology, their applications in cardiac drug development and tissue repair, and how these models can advance cardiovascular research.</div></div>","PeriodicalId":100900,"journal":{"name":"Mechanobiology in Medicine","volume":"3 3","pages":"Article 100144"},"PeriodicalIF":0.0,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144535580","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}
Gurneet S. Sangha , Lauren V. Smith , Marzyeh Kheradmand , Kashif M. Munir , Nimisha Rangachar , Callie M. Weber , Zohreh Safari , Stephen C. Rogers , Allan Doctor , Alisa Morss Clyne
{"title":"Piezo1 activates nitric oxide synthase in red blood cells via protein kinase C with increased activity in diabetes","authors":"Gurneet S. Sangha , Lauren V. Smith , Marzyeh Kheradmand , Kashif M. Munir , Nimisha Rangachar , Callie M. Weber , Zohreh Safari , Stephen C. Rogers , Allan Doctor , Alisa Morss Clyne","doi":"10.1016/j.mbm.2025.100145","DOIUrl":"10.1016/j.mbm.2025.100145","url":null,"abstract":"<div><div>Nitric oxide (NO) is a key signaling molecule in maintaining cardiovascular health. While endothelial cells were initially thought to exclusively contain endothelial nitric oxide synthase (eNOS), an enzyme that produces NO, recent evidence suggests that red blood cells (RBC) also contain functional eNOS that impacts cardiovascular function. However, the mechanisms driving RBC eNOS activation are not well understood. Like endothelial cells, RBC are mechanosensitive via the stretch-activated piezo1 Ca<sup>2+</sup> channel. Therefore, we investigated how piezo1 stimulation induced RBC and endothelial eNOS phosphorylation. We further examined how this mechanism is affected during diabetes, a condition known to impair vascular NO bioavailability. Our results reveal that piezo1 stimulation activated RBC eNOS via protein kinase C (PKC) and endothelial eNOS partially via protein kinase B (Akt). Surprisingly, piezo1-stimulation increased eNOS phosphorylation at the Ser1177 activation site nearly 20-fold in RBC from diabetic patients compared to 5.5-fold in RBC from non-diabetic patients. These findings highlight important differences in eNOS activation between RBC and endothelial cells and suggest potential biomolecular markers for targeting vascular NO bioavailability in health and disease.</div></div>","PeriodicalId":100900,"journal":{"name":"Mechanobiology in Medicine","volume":"3 3","pages":"Article 100145"},"PeriodicalIF":0.0,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144771986","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}
Shaotian Fu , Yahong Lu , Wenkun Sun , Wugui Chen , Chengshou Lin , An Qin
{"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":"2025-06-01","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}
Bingtong Yan , Minmin Lin , Yang Liu , Jiawei Li , Linjing Peng , Yifei Yao , Guangheng Li , Chao Liu
{"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":"2025-06-01","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}