Mechanobiology in Medicine最新文献

Magnesium-containing implants enhance bone healing: A mechanobiological perspective

Mechanobiology in Medicine Pub Date : 2025-10-20 DOI: 10.1016/j.mbm.2025.100161

Zhenkang Wen , Lei Lei , Haozhi Zhang , Zheyu Jin , Zhengming Shan , Weiyang Liu , Wenxue Tong , Jiankun Xu , Ling Qin

{"title":"Magnesium-containing implants enhance bone healing: A mechanobiological perspective","authors":"Zhenkang Wen , Lei Lei , Haozhi Zhang , Zheyu Jin , Zhengming Shan , Weiyang Liu , Wenxue Tong , Jiankun Xu , Ling Qin","doi":"10.1016/j.mbm.2025.100161","DOIUrl":"10.1016/j.mbm.2025.100161","url":null,"abstract":"<div><div>Unlike traditional implants primarily composed of bioinert materials, magnesium (Mg) -a degradable biomaterial - offers significant promise for next-generation bone healing implants, whether utilized as a primary structural component or a supporting material. While most research focuses on Mg's bioactive and osteoimmunological effect, this review highlights its mechanobiological role, summarizing the merits of Mg-containing implants in facilitating mechanotransduction and associated cellular events during the bone healing. Beyond introducing Mg's biomechanical benefits in preventing stress shielding, this review synthesizes its unique attributes: exceptional bone-implant integration and synergistic effects with physical stimuli to amplify new bone formation. Crucially, we also summarize the activation of mechanotransduction signaling pathways, providing a mechanistic basis for Mg's positive mechanobiological influence. Finally, we discuss challenges arising from the interaction between physical loading and Mg degradation, alongside future perspectives and potential solutions to bridge the gap between theory and clinical application, thereby accelerating translation applications of Mg-containing implants.</div></div>","PeriodicalId":100900,"journal":{"name":"Mechanobiology in Medicine","volume":"3 4","pages":"Article 100161"},"PeriodicalIF":0.0,"publicationDate":"2025-10-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145363506","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

Synthetic mechanoreceptor engineering: From genetic encoding to DNA nanotechnology-based reprogramming 合成机械受体工程：从遗传编码到基于DNA纳米技术的重编程

Mechanobiology in Medicine Pub Date : 2025-10-06 DOI: 10.1016/j.mbm.2025.100160

Sihui Yang , Zhou Nie

{"title":"Synthetic mechanoreceptor engineering: From genetic encoding to DNA nanotechnology-based reprogramming","authors":"Sihui Yang , Zhou Nie","doi":"10.1016/j.mbm.2025.100160","DOIUrl":"10.1016/j.mbm.2025.100160","url":null,"abstract":"<div><div>Precise modulation of mechanoreceptor-mediated signal transduction is crucial for decoding cellular mechanotransduction mechanisms and programming cell fate. This review provides a comprehensive summary of recent advances in engineering synthetic mechanoreceptors, spanning from protein-centric genetic encoding to DNA nanotechnology-based non-genetic reprogramming strategies. Genetic engineering strategies employ protein structure encoding and site-directed mutagenesis to reprogram force-response functions in natural mechanoreceptors. As a complementary non-genetic approach, DNA nanotechnology leverages its programmability, modularity, and predictable mechanical properties to achieve precise control over receptor functionalities. The flourishing development of DNA mechanosensitive nanodevices has provided a promising synthetic toolkit for manipulating mechanoreceptors, enabling precise control over receptor spatial organization and signal transduction. A key innovation is the development of novel DNA-functionalized artificial mechanoreceptors (AMRs), which confer force-responsiveness to naturally non-mechanosensitive receptors without genetic modification, thereby enabling customized mechanotransduction and mechanobiological applications. Collectively, this paradigm shift highlights DNA-based non-genetic receptor engineering as a versatile and powerful toolkit, paving new avenues for mechanobiology research and pioneering force-directed therapeutic strategies in regenerative medicine.</div></div>","PeriodicalId":100900,"journal":{"name":"Mechanobiology in Medicine","volume":"3 4","pages":"Article 100160"},"PeriodicalIF":0.0,"publicationDate":"2025-10-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145321156","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

Multimodal mechanoregulation strategies towards tissue regeneration 组织再生的多模式机械调控策略

Mechanobiology in Medicine Pub Date : 2025-09-25 DOI: 10.1016/j.mbm.2025.100159

Qifan Yu , Yudong Duan , Zhuang Zhu , Wei Ji , Caihong Zhu , Bin Li

{"title":"Multimodal mechanoregulation strategies towards tissue regeneration","authors":"Qifan Yu , Yudong Duan , Zhuang Zhu , Wei Ji , Caihong Zhu , Bin Li","doi":"10.1016/j.mbm.2025.100159","DOIUrl":"10.1016/j.mbm.2025.100159","url":null,"abstract":"<div><div>Mechanical microenvironment of each tissue plays an important role in regulating its special cellular behaviors, such as morphology, proliferation, differentiation, and migration. Mechanical signals can direct lineage specification or promote cell migration towards injury sites and facilitate tissue repair. During tissue regeneration, mechanoregulation is also important due to the ability of providing an extracellular microenvironment that closely resembles the physiological state for cells. Currently, mechanoregulation strategies have been usually applied to promote tissue regeneration. However, the <em>in vivo</em> mechanical environment is highly complex, these single mechanical conditioning strategies cannot comprehensively replicate the mechanical microenvironment experienced by cells or tissues in the body, thereby hindering the achievement of efficient tissue regeneration. The proposal of multimodal mechanoregulation strategies offers promising avenues to address this limitation. Herein, we summarize the critical role of mechanical factors in promoting tissue regeneration and the current development of different multimodal mechanoregulation approaches. Furthermore, the complex mechanical microenvironment of various tissues such as bone, intervertebral disc and cardiac. Afterwards, the recent successful applications of multimodal mechanical strategies in regenerative therapies were reviewed. And we delineate the persisting challenges, potential resolutions, and emerging translational prospects for multimodal mechanoregulation strategies in regenerative medicine, providing a reference for further development of multimodal mechanoregulation approaches.</div></div>","PeriodicalId":100900,"journal":{"name":"Mechanobiology in Medicine","volume":"3 4","pages":"Article 100159"},"PeriodicalIF":0.0,"publicationDate":"2025-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145321157","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

Substrate stiffness modulates phenotype-dependent fibroblast contractility and migration independent of TGF-β stimulation 底物硬度调节表型依赖性成纤维细胞的收缩性和迁移，独立于TGF-β刺激

Mechanobiology in Medicine Pub Date : 2025-09-24 DOI: 10.1016/j.mbm.2025.100158

Mirko D'Urso , Pim van den Bersselaar , Sarah Pragnere , Paolo Maiuri , Carlijn V.C. Bouten , Nicholas A. Kurniawan

{"title":"Substrate stiffness modulates phenotype-dependent fibroblast contractility and migration independent of TGF-β stimulation","authors":"Mirko D'Urso , Pim van den Bersselaar , Sarah Pragnere , Paolo Maiuri , Carlijn V.C. Bouten , Nicholas A. Kurniawan","doi":"10.1016/j.mbm.2025.100158","DOIUrl":"10.1016/j.mbm.2025.100158","url":null,"abstract":"<div><div>During wound healing, fibroblasts undergo radical processes that impact their phenotype and behavior. They are activated, recruited to the injury site, assume a contractile phenotype, and secrete extracellular matrix proteins to orchestrate tissue repair. Thus, fibroblast responses require dynamic changes in cytoskeleton assembly and organization, adhesion morphology, and force generation. At the same time, fibroblasts experience changes in environmental stiffness during tissue wounding and healing. Although cells are generally known to use their adhesion–contraction machinery to sense microenvironmental stiffness, little is known about how stiffness affects the fibroblast phenotypical transition and behavior in wound healing. Here we demonstrate that stiffness plays a deterministic role in determining fibroblast phenotype, surprisingly even overruling the classical TGF-<em>β</em>-mediated stimulation. By combining morphometric analysis, traction force microscopy, and single-cell migration analysis, we show that environmental stiffness primes the cytoskeletal and mechanical responses of fibroblasts, strongly modulating their morphology, force generation, and migration behavior. Our study, therefore, points to the importance of tissue stiffness as a key mechanobiological regulator of fibroblast behavior, thus serving as a potential target for controlling tissue repair.</div></div>","PeriodicalId":100900,"journal":{"name":"Mechanobiology in Medicine","volume":"3 4","pages":"Article 100158"},"PeriodicalIF":0.0,"publicationDate":"2025-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145221328","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

Mechanotransduction in neutrophil: Mechanosensing and immune function regulation 中性粒细胞的机械转导：机械感应和免疫功能调节

Mechanobiology in Medicine Pub Date : 2025-09-07 DOI: 10.1016/j.mbm.2025.100157

Wenying Zhao, Jin Wang, Jing Wang

引用次数: 0

Allosteric pockets in the measles and Nipah virus polymerases: Mechanobiological insights and AI-driven drug discovery opportunities 麻疹和尼帕病毒聚合酶的变构口袋：机械生物学见解和人工智能驱动的药物发现机会

Mechanobiology in Medicine Pub Date : 2025-08-26 DOI: 10.1016/j.mbm.2025.100156

Yiru Wang , Lixia Zhao , Heqiao Zhang

引用次数: 0

Theta-shaking mitigates cognitive-emotional decline via subiculum and ventral septum metabolic plasticity 脑波震动通过枕下和腹隔代谢可塑性减轻认知情绪下降

Mechanobiology in Medicine Pub Date : 2025-08-22 DOI: 10.1016/j.mbm.2025.100148

Runhong Yao , Kouji Yamada , Hirohide Sawada , Takeshi Chihara , Naoki Aizu , Kazuhiro Nishii

{"title":"Theta-shaking mitigates cognitive-emotional decline via subiculum and ventral septum metabolic plasticity","authors":"Runhong Yao , Kouji Yamada , Hirohide Sawada , Takeshi Chihara , Naoki Aizu , Kazuhiro Nishii","doi":"10.1016/j.mbm.2025.100148","DOIUrl":"10.1016/j.mbm.2025.100148","url":null,"abstract":"<div><div>Aging-associated cognitive decline remains a major challenge in gerontology; few non-invasive interventions provide both mechanistic insight and translational feasibility. We investigated whether low-frequency “theta-shaking” whole-body vibration (5 Hz) could modulate cognitive function, emotional behavior, and metabolic plasticity in a senescence-accelerated mouse model. Senescence-accelerated mouse prone-10 mice were exposed to theta-shaking stimulation for 30 weeks. Spatial memory was assessed using Y-maze spontaneous alternation test, and anxiety-related behavior was evaluated using marble burying test. Histological and immunohistochemical analyses were conducted to assess neuronal density and protein expression in specific brain regions. Theta-shaking subjected mice exhibited delayed yet significant improvements in spatial memory at 20 (p = 0.017) and 30 (p = 0.018) weeks. Anxiety-related behavior shows a biphasic pattern: an initial increase at 20 weeks (p < 0.001) followed by stabilization at 30 weeks. Histological analysis revealed preserved neuronal density in the subiculum (p < 0.001) and elevated proliferator-activated receptor gamma coactivator 1-alpha (PGC1α) expression in the Cornu Ammonis 1, subiculum, and lateral septum (all p < 0.05). Notably, mitochondrial biogenesis appeared to be intervention's primary target, as shown by robust PGC1α upregulation, while brain-derived neurotrophic factor revealed a trend-level increase (p = 0.062), and neurotrophin-3 expression remained unchanged. Frequency-tuned mechanical stimulation induced region-specific neural neurometabolic adaptations, supporting theta-shaking as a non-pharmacological, low-exertion strategy to counteract brain aging. These findings offer promising translational potential, especially for individuals with limited mobility.</div></div>","PeriodicalId":100900,"journal":{"name":"Mechanobiology in Medicine","volume":"3 4","pages":"Article 100148"},"PeriodicalIF":0.0,"publicationDate":"2025-08-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145020550","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

Fighting cardiac fibrosis using the chemomechanical method 利用化学力学方法对抗心脏纤维化

Mechanobiology in Medicine Pub Date : 2025-08-16 DOI: 10.1016/j.mbm.2025.100147

Yunlong Huo

引用次数: 0

Mitochondria power the nucleus under pressure 线粒体在压力下为细胞核提供能量

Mechanobiology in Medicine Pub Date : 2025-08-12 DOI: 10.1016/j.mbm.2025.100146

Meng Yao , Yao Zong , Junjie Gao

{"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":"2025-08-12","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}

引用次数: 0

Piezo1 activates nitric oxide synthase in red blood cells via protein kinase C with increased activity in diabetes Piezo1通过蛋白激酶C激活红细胞中的一氧化氮合酶，并在糖尿病中增加活性

Mechanobiology in Medicine Pub Date : 2025-07-28 DOI: 10.1016/j.mbm.2025.100145

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":"2025-07-28","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}

引用次数: 0