Pub Date : 2026-01-07DOI: 10.1016/j.mbm.2026.100174
Jessy V. van Asperen , Elly M. Hol
Glioblastoma (GBM) is a highly invasive tumour. Invasion of GBM cells into the densely packed brain parenchyma reflects a profound mechanobiological adaptation to the mechanical constraints of the brain. A recent study by van Bodegraven et al. (https://doi.org/10.1016/j.celrep.2025.116553) positions intermediate filaments as central regulators of this mechanoadaptive response. The intermediate filament perinuclear cage decreases the deformability of the cell and therewith the deformability of the nucleus. Despite of this, the presence of intermediate filaments leads to a greater invasive capacity due to mechanosensitive upregulation of metalloproteinase 14 and increased extracellular matrix degradation. The enrichment of intermediate filament transcripts in GBM patient cells with pro-invasive markers indicates that intermediate filaments contribute to the specialization of GBM cells towards invasive behavior. This work fits within an emerging paradigm in which intermediate filament expression is viewed as being tailored to the mechanical demands of the invading cell.
{"title":"A tailored fit: How intermediate filaments orchestrate glioblastoma invasion","authors":"Jessy V. van Asperen , Elly M. Hol","doi":"10.1016/j.mbm.2026.100174","DOIUrl":"10.1016/j.mbm.2026.100174","url":null,"abstract":"<div><div>Glioblastoma (GBM) is a highly invasive tumour. Invasion of GBM cells into the densely packed brain parenchyma reflects a profound mechanobiological adaptation to the mechanical constraints of the brain. A recent study by van Bodegraven et al. (<span><span>https://doi.org/10.1016/j.celrep.2025.116553</span><svg><path></path></svg></span>) positions intermediate filaments as central regulators of this mechanoadaptive response. The intermediate filament perinuclear cage decreases the deformability of the cell and therewith the deformability of the nucleus. Despite of this, the presence of intermediate filaments leads to a greater invasive capacity due to mechanosensitive upregulation of metalloproteinase 14 and increased extracellular matrix degradation. The enrichment of intermediate filament transcripts in GBM patient cells with pro-invasive markers indicates that intermediate filaments contribute to the specialization of GBM cells towards invasive behavior. This work fits within an emerging paradigm in which intermediate filament expression is viewed as being tailored to the mechanical demands of the invading cell.</div></div>","PeriodicalId":100900,"journal":{"name":"Mechanobiology in Medicine","volume":"4 1","pages":"Article 100174"},"PeriodicalIF":0.0,"publicationDate":"2026-01-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145977238","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 : 2025-12-31DOI: 10.1016/j.mbm.2025.100173
Shiqi Hu , Buwei Hu , Jing Yang , Rui Liu , Yang Song , Yufan Zheng
Penicillin–streptomycin (pen-strep) is routinely included in cell culture media, yet its impact on macrophage mechanics has not been systematically examined. Here, we show that pen-strep treatment increases macrophage stiffness in a time-dependent manner, while adhesion strength is only transiently affected. Morphological analysis revealed that pen-strep promotes cell spreading on PDMS rubber, collagen I, laminin, poly-amino acids, and poly-RGD peptides, but reduces spreading on type IV collagen, indicating altered extracellular matrix sensing in a context-dependent fashion. Gene expression assays further demonstrated upregulation of YAP-1 and TAZ and downregulation of β1 integrin, consistent with reprogramming of mechanotransduction pathways. Consequently, pen-strep elevated intracellular ROS, suppressed the M1 gene spectrum, induced heterogeneous M2-associated responses, and impaired phagocytic capacity. Collectively, these findings identify pen-strep as a modulator of macrophage stiffness, ECM mechano-sensation, polarization, and key immune functions, raising concerns about its routine use in mechanobiology research and clinical applications.
{"title":"Penicillin–streptomycin influences macrophage mechanical properties and microenvironment mechano-sensation1","authors":"Shiqi Hu , Buwei Hu , Jing Yang , Rui Liu , Yang Song , Yufan Zheng","doi":"10.1016/j.mbm.2025.100173","DOIUrl":"10.1016/j.mbm.2025.100173","url":null,"abstract":"<div><div>Penicillin–streptomycin (pen-strep) is routinely included in cell culture media, yet its impact on macrophage mechanics has not been systematically examined. Here, we show that pen-strep treatment increases macrophage stiffness in a time-dependent manner, while adhesion strength is only transiently affected. Morphological analysis revealed that pen-strep promotes cell spreading on PDMS rubber, collagen I, laminin, poly-amino acids, and poly-RGD peptides, but reduces spreading on type IV collagen, indicating altered extracellular matrix sensing in a context-dependent fashion. Gene expression assays further demonstrated upregulation of YAP-1 and TAZ and downregulation of β1 integrin, consistent with reprogramming of mechanotransduction pathways. Consequently, pen-strep elevated intracellular ROS, suppressed the M1 gene spectrum, induced heterogeneous M2-associated responses, and impaired phagocytic capacity. Collectively, these findings identify pen-strep as a modulator of macrophage stiffness, ECM mechano-sensation, polarization, and key immune functions, raising concerns about its routine use in mechanobiology research and clinical applications.</div></div>","PeriodicalId":100900,"journal":{"name":"Mechanobiology in Medicine","volume":"4 1","pages":"Article 100173"},"PeriodicalIF":0.0,"publicationDate":"2025-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145939110","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 : 2025-12-02DOI: 10.1016/j.mbm.2025.100166
Cheng Zhu
The immune system relies on intricate molecular interactions and cellular signaling to discriminate between self and non-self, mount appropriate responses to pathogens and cancer, and maintain tissue homeostasis to avoid autoimmune diseases. Evidence increasingly supports the critical role of mechanical forces in regulating immune cell function and differentiation through immunoreceptor interactions with immobilized ligands, leading to the emerging interdisciplinary field of mechanoimmunology. This review delves into the historical development and recent advances of the field. We highlight the key concepts and questions in understanding how immune cells perceive and respond to mechanical cues, with a focus on the critical role of catch bonds in immunoreceptor-mediated mechanotransduction and explore their immunotherapeutic applications. Furthermore, we explore the profound implications of mechanoimmunology for understanding major immunological problems and its potential applications in advanced immunotherapies and regenerative medicine.
{"title":"Mechanoimmunology: past, present, and future perspectives","authors":"Cheng Zhu","doi":"10.1016/j.mbm.2025.100166","DOIUrl":"10.1016/j.mbm.2025.100166","url":null,"abstract":"<div><div>The immune system relies on intricate molecular interactions and cellular signaling to discriminate between self and non-self, mount appropriate responses to pathogens and cancer, and maintain tissue homeostasis to avoid autoimmune diseases. Evidence increasingly supports the critical role of mechanical forces in regulating immune cell function and differentiation through immunoreceptor interactions with immobilized ligands, leading to the emerging interdisciplinary field of mechanoimmunology. This review delves into the historical development and recent advances of the field. We highlight the key concepts and questions in understanding how immune cells perceive and respond to mechanical cues, with a focus on the critical role of catch bonds in immunoreceptor-mediated mechanotransduction and explore their immunotherapeutic applications. Furthermore, we explore the profound implications of mechanoimmunology for understanding major immunological problems and its potential applications in advanced immunotherapies and regenerative medicine.</div></div>","PeriodicalId":100900,"journal":{"name":"Mechanobiology in Medicine","volume":"4 1","pages":"Article 100166"},"PeriodicalIF":0.0,"publicationDate":"2025-12-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145750141","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 : 2025-12-01DOI: 10.1016/j.mbm.2025.100164
Gaige Wu , Shuai Chen , Qian Li , Min Zhang , Fuyang Cao , Junchao Wei , Li Guo , Pengcui Li , Xiaochun Wei , Quanyou Zhang
Chondrocytes, the sole cell type in articular cartilage, are responsible for synthesizing and maintaining the primary components of the extracellular matrix (ECM). In daily life, chondrocytes are subjected to diverse mechanical stimuli, and the mechanoregulation of their biological responses plays a crucial role in cartilage function. Chondrocytes exhibit remarkable mechanoadaptation, as mechanical stimulation effectively promotes their homeostasis, development, and regeneration—critical factors for regenerative medicine. Thus, a deeper understanding of chondrocyte mechanosensing mechanism is essential. A key challenge lies in the significant biomechanical heterogeneity of chondrocytes across developmental stages and spatial locations of articular cartilage, leading to variations in their mechanosensing and mechanoresponsive behaviors. Elucidating the spatiotemporal biomechanical properties of chondrocytes is of great importance. Mechanical cues regulate chondrocyte homeostasis through multidimensional mechanisms, enhance energy metabolism, and dynamically couple with the cytoskeleton to optimize their responsiveness to matrix mechanical microenvironment. However, under pathological conditions, the aberrant mechanosensing of chondrocyte exacerbates inflammatory responses and matrix degradation, which further deteriorating the mechanical microenvironment. Growing evidence has indicated that some critical factors include dysregulated activation of mechanosensitive ion channels, disrupted integrin signaling pathways, and structural damage to primary cilia induce abnormal chondrocyte function. Biomechanical intervention strategies, such as mechanical loading techniques and exercise-based rehabilitation, hold promising potential for cartilage repair and regeneration by reconstructing the physiological-related mechanical microenvironment. This review provides a theoretical foundation for understanding the mechanisms of cartilage degenerative diseases and developing targeted therapies from a mechanobiological perspective.
{"title":"Mechanical cues enhance chondrocyte function: Insights from mechanoreception, regulation, and biological responses","authors":"Gaige Wu , Shuai Chen , Qian Li , Min Zhang , Fuyang Cao , Junchao Wei , Li Guo , Pengcui Li , Xiaochun Wei , Quanyou Zhang","doi":"10.1016/j.mbm.2025.100164","DOIUrl":"10.1016/j.mbm.2025.100164","url":null,"abstract":"<div><div>Chondrocytes, the sole cell type in articular cartilage, are responsible for synthesizing and maintaining the primary components of the extracellular matrix (ECM). In daily life, chondrocytes are subjected to diverse mechanical stimuli, and the mechanoregulation of their biological responses plays a crucial role in cartilage function. Chondrocytes exhibit remarkable mechanoadaptation, as mechanical stimulation effectively promotes their homeostasis, development, and regeneration—critical factors for regenerative medicine. Thus, a deeper understanding of chondrocyte mechanosensing mechanism is essential. A key challenge lies in the significant biomechanical heterogeneity of chondrocytes across developmental stages and spatial locations of articular cartilage, leading to variations in their mechanosensing and mechanoresponsive behaviors. Elucidating the spatiotemporal biomechanical properties of chondrocytes is of great importance. Mechanical cues regulate chondrocyte homeostasis through multidimensional mechanisms, enhance energy metabolism, and dynamically couple with the cytoskeleton to optimize their responsiveness to matrix mechanical microenvironment. However, under pathological conditions, the aberrant mechanosensing of chondrocyte exacerbates inflammatory responses and matrix degradation, which further deteriorating the mechanical microenvironment. Growing evidence has indicated that some critical factors include dysregulated activation of mechanosensitive ion channels, disrupted integrin signaling pathways, and structural damage to primary cilia induce abnormal chondrocyte function. Biomechanical intervention strategies, such as mechanical loading techniques and exercise-based rehabilitation, hold promising potential for cartilage repair and regeneration by reconstructing the physiological-related mechanical microenvironment. This review provides a theoretical foundation for understanding the mechanisms of cartilage degenerative diseases and developing targeted therapies from a mechanobiological perspective.</div></div>","PeriodicalId":100900,"journal":{"name":"Mechanobiology in Medicine","volume":"3 4","pages":"Article 100164"},"PeriodicalIF":0.0,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145617841","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 : 2025-12-01DOI: 10.1016/j.mbm.2025.100162
Han Qiao , Kai Zhang , Jie Zhao
Intervertebral disc degeneration (IVDD) is a complex mechanobiological process driven by abnormal mechanical loading, resulting in structural failure, inflammatory activation, and cellular dysfunction. Understanding these mechanobiological interactions offers novel therapeutic targets to interrupt the degenerative cascade and improve clinical outcomes in IVDD treatment. This review summarizes the fundamental characteristics of the mechanobiological microenvironment in IVDD, detailing mechanosensitive spinal components and providing evidence for mechanobiology-based therapies. By enhancing insight into disc degeneration from a mechanobiological perspective, researchers can develop innovative therapeutic strategies to restore a healthy disc microenvironment and spinal stability clinically, offering a promising outlook for patients with IVDD. However, current studies primarily focus on in vitro models and in vivo animal studies, limiting clinical translation. Therefore, effectively translating these research findings into practical clinical treatments remains a notable future challenge.
{"title":"Mechanobiology of intervertebral disc degeneration: From pathological mechanisms to therapeutic approaches","authors":"Han Qiao , Kai Zhang , Jie Zhao","doi":"10.1016/j.mbm.2025.100162","DOIUrl":"10.1016/j.mbm.2025.100162","url":null,"abstract":"<div><div>Intervertebral disc degeneration (IVDD) is a complex mechanobiological process driven by abnormal mechanical loading, resulting in structural failure, inflammatory activation, and cellular dysfunction. Understanding these mechanobiological interactions offers novel therapeutic targets to interrupt the degenerative cascade and improve clinical outcomes in IVDD treatment. This review summarizes the fundamental characteristics of the mechanobiological microenvironment in IVDD, detailing mechanosensitive spinal components and providing evidence for mechanobiology-based therapies. By enhancing insight into disc degeneration from a mechanobiological perspective, researchers can develop innovative therapeutic strategies to restore a healthy disc microenvironment and spinal stability clinically, offering a promising outlook for patients with IVDD. However, current studies primarily focus on in vitro models and in vivo animal studies, limiting clinical translation. Therefore, effectively translating these research findings into practical clinical treatments remains a notable future challenge.</div></div>","PeriodicalId":100900,"journal":{"name":"Mechanobiology in Medicine","volume":"3 4","pages":"Article 100162"},"PeriodicalIF":0.0,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145617842","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 : 2025-11-21DOI: 10.1016/j.mbm.2025.100165
Yunjia Qu , Jiaxin Cui , Zhuohang Wu , Peixiang He , Fan Wei , Tianze Guo , Yixuan Huang , Xi Yu , Mishel Tsoy , Kunshu Liu , Ziyue Zhu , Yiming Zhang , Yingxiao Wang , Longwei Liu
Cancer cell memory, the ability to retain responses to prior environmental stimuli, has emerged as a key driver of tumor progression, therapeutic resistance, and immune evasion. Mechanical cues within the tumor microenvironment (TME), including matrix stiffness, viscoelasticity, and compressive stress, are increasingly recognized as critical regulators of such memory. These biophysical inputs not only influence immediate cellular behavior but also induce long-lasting transcriptional, epigenetic, and phenotypic changes that sustain cancer cell aggressive traits. In this review, we specifically highlight mechanobiology in shaping cancer cell memory. We summarize how extracellular matrix (ECM) composition and remodeling encodes mechanical inputs into stable gene expression programs that promote tumor progression, and highlight how mechano-regulated plasticity, membrane tension, chromatin remodeling, and epigenetic changes govern self-renewal, differentiation, and drug and immune resistance, underscoring how physical suppression contributes to chemo-, radio-, and targeted therapies failure. We further discuss emerging mechano-targeted strategies, including ECM-degrading agents, sonogenetic engineered cells, and stiffness-responsive nanoparticles, that seek to rewire cancer cell memory and improve treatment outcomes.
{"title":"Mechano-regulation of cancer cell memory in tumor progression and therapy","authors":"Yunjia Qu , Jiaxin Cui , Zhuohang Wu , Peixiang He , Fan Wei , Tianze Guo , Yixuan Huang , Xi Yu , Mishel Tsoy , Kunshu Liu , Ziyue Zhu , Yiming Zhang , Yingxiao Wang , Longwei Liu","doi":"10.1016/j.mbm.2025.100165","DOIUrl":"10.1016/j.mbm.2025.100165","url":null,"abstract":"<div><div>Cancer cell memory, the ability to retain responses to prior environmental stimuli, has emerged as a key driver of tumor progression, therapeutic resistance, and immune evasion. Mechanical cues within the tumor microenvironment (TME), including matrix stiffness, viscoelasticity, and compressive stress, are increasingly recognized as critical regulators of such memory. These biophysical inputs not only influence immediate cellular behavior but also induce long-lasting transcriptional, epigenetic, and phenotypic changes that sustain cancer cell aggressive traits. In this review, we specifically highlight mechanobiology in shaping cancer cell memory. We summarize how extracellular matrix (ECM) composition and remodeling encodes mechanical inputs into stable gene expression programs that promote tumor progression, and highlight how mechano-regulated plasticity, membrane tension, chromatin remodeling, and epigenetic changes govern self-renewal, differentiation, and drug and immune resistance, underscoring how physical suppression contributes to chemo-, radio-, and targeted therapies failure. We further discuss emerging mechano-targeted strategies, including ECM-degrading agents, sonogenetic engineered cells, and stiffness-responsive nanoparticles, that seek to rewire cancer cell memory and improve treatment outcomes.</div></div>","PeriodicalId":100900,"journal":{"name":"Mechanobiology in Medicine","volume":"4 1","pages":"Article 100165"},"PeriodicalIF":0.0,"publicationDate":"2025-11-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145694823","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 : 2025-11-04DOI: 10.1016/j.mbm.2025.100163
Jixing Miao , Mingjie Ma , Yuhan Guo , Ling Qin , Lutian Yao
Spatial transcriptomics analysis of mineralized tissues faces significant challenges due to lengthy decalcification procedures that severely compromise RNA integrity and subsequent gene detection. This protocol details an optimized workflow to process bone and fracture callus samples for 10x Genomics Visium spatial transcriptomics. The key innovation involves replacing conventional EDTA decalcification with Morse's solution, enabling rapid decalcification (<24 h) while preserving RNA quality, as evidenced by a favorable DV200 value. Additionally, the protocol emphasizes the critical use of SCHOTT NEXTERION® Slide H (3-D hydrogel-coated) to maximize adherence of fragile decalcified bone sections during processing, preventing detachment and preserving morphological integrity. We applied this optimized method to intact and fractured mouse femurs. The results demonstrate a substantial improvement in transcript capture efficiency: Visium V2 yielded an average of 5639 genes per spot, while Visium HD achieved an average of 170 genes per 8 μm bin (equivalent to ∼4100 genes per 55 μm spot). This step-by-step protocol overcomes major pre-analytical hurdles, enabling high-resolution spatial transcriptomic profiling of mineralized tissues with significantly enhanced data quality.
{"title":"A practical protocol of processing mineralized tissue for Visium spatial transcriptomics","authors":"Jixing Miao , Mingjie Ma , Yuhan Guo , Ling Qin , Lutian Yao","doi":"10.1016/j.mbm.2025.100163","DOIUrl":"10.1016/j.mbm.2025.100163","url":null,"abstract":"<div><div>Spatial transcriptomics analysis of mineralized tissues faces significant challenges due to lengthy decalcification procedures that severely compromise RNA integrity and subsequent gene detection. This protocol details an optimized workflow to process bone and fracture callus samples for 10x Genomics Visium spatial transcriptomics. The key innovation involves replacing conventional EDTA decalcification with Morse's solution, enabling rapid decalcification (<24 h) while preserving RNA quality, as evidenced by a favorable DV200 value. Additionally, the protocol emphasizes the critical use of SCHOTT NEXTERION® Slide H (3-D hydrogel-coated) to maximize adherence of fragile decalcified bone sections during processing, preventing detachment and preserving morphological integrity. We applied this optimized method to intact and fractured mouse femurs. The results demonstrate a substantial improvement in transcript capture efficiency: Visium V2 yielded an average of 5639 genes per spot, while Visium HD achieved an average of 170 genes per 8 μm bin (equivalent to ∼4100 genes <em>per</em> 55 μm spot). This step-by-step protocol overcomes major pre-analytical hurdles, enabling high-resolution spatial transcriptomic profiling of mineralized tissues with significantly enhanced data quality.</div></div>","PeriodicalId":100900,"journal":{"name":"Mechanobiology in Medicine","volume":"3 4","pages":"Article 100163"},"PeriodicalIF":0.0,"publicationDate":"2025-11-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145519778","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 : 2025-10-20DOI: 10.1016/j.mbm.2025.100161
Zhenkang Wen , Lei Lei , Haozhi Zhang , Zheyu Jin , Zhengming Shan , Weiyang Liu , Wenxue Tong , Jiankun Xu , Ling Qin
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.
{"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}
Pub Date : 2025-10-06DOI: 10.1016/j.mbm.2025.100160
Sihui Yang , Zhou Nie
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.
{"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}
Pub Date : 2025-09-25DOI: 10.1016/j.mbm.2025.100159
Qifan Yu , Yudong Duan , Zhuang Zhu , Wei Ji , Caihong Zhu , Bin Li
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 in vivo 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.
{"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}
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