Pub Date : 2025-12-01Epub Date: 2025-09-07DOI: 10.1016/j.mbm.2025.100157
Wenying Zhao, Jin Wang, Jing Wang
Immune cells sense and transduce mechanical signals such as stiffness, stretch, compression, and shear stress. In the past few years, our understanding of the mechanosensitive signaling pathways in myeloid cells has significantly expanded, especially in monocytes, macrophages, and dendritic cells. Recently, the mechanobiological regulation of neutrophil function has been deciphered. Mechanical signals from tissue-derived shear stress and cellular deformation tension reprogram neutrophil transcription via GEF-H1, PIEZO1, and TRPV4 pathways, modulating neutrophil functions in homeostasis and trans-endothelial migration. Understanding these force-dependent processes provides novel insights into neutrophil plasticity and highlights potential therapeutic strategies and approaches for inflammatory and infectious diseases.
{"title":"Mechanotransduction in neutrophil: Mechanosensing and immune function regulation","authors":"Wenying Zhao, Jin Wang, Jing Wang","doi":"10.1016/j.mbm.2025.100157","DOIUrl":"10.1016/j.mbm.2025.100157","url":null,"abstract":"<div><div>Immune cells sense and transduce mechanical signals such as stiffness, stretch, compression, and shear stress. In the past few years, our understanding of the mechanosensitive signaling pathways in myeloid cells has significantly expanded, especially in monocytes, macrophages, and dendritic cells. Recently, the mechanobiological regulation of neutrophil function has been deciphered. Mechanical signals from tissue-derived shear stress and cellular deformation tension reprogram neutrophil transcription via GEF-H1, PIEZO1, and TRPV4 pathways, modulating neutrophil functions in homeostasis and trans-endothelial migration. Understanding these force-dependent processes provides novel insights into neutrophil plasticity and highlights potential therapeutic strategies and approaches for inflammatory and infectious diseases.</div></div>","PeriodicalId":100900,"journal":{"name":"Mechanobiology in Medicine","volume":"3 4","pages":"Article 100157"},"PeriodicalIF":0.0,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145061097","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 : 2025-12-01Epub Date: 2025-11-19DOI: 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 : 2025-12-01Epub Date: 2025-08-26DOI: 10.1016/j.mbm.2025.100156
Yiru Wang , Lixia Zhao , Heqiao Zhang
Nonsegmented negative-sense RNA viruses (nsNSVs)—including highly pathogenic pathogens such as measles virus (MeV), Nipah virus (NiV), Hendra virus (HeV), Ebola virus (EBOV), and others—pose major global health threats, yet most lack approved antiviral therapeutics. In the recent study, high-resolution cryo-electron microscopy (cryo-EM) revealed previously unrecognized allosteric pockets in the large (L) polymerase proteins of MeV and NiV, spatially distinct from the catalytic nucleotide-binding site. We further demonstrated that the non-nucleoside inhibitor ERDRP-0519 engages these pockets to allosterically ‘lock’ the polymerase in a mechanically inactive state. These findings reveal an allosteric mechanism of inhibition rooted in the conformational mechanics of the enzyme and highlight opportunities for integrating artificial intelligence (AI)-aided drug discovery (AIDD) into rational drug design.
{"title":"Allosteric pockets in the measles and Nipah virus polymerases: Mechanobiological insights and AI-driven drug discovery opportunities","authors":"Yiru Wang , Lixia Zhao , Heqiao Zhang","doi":"10.1016/j.mbm.2025.100156","DOIUrl":"10.1016/j.mbm.2025.100156","url":null,"abstract":"<div><div>Nonsegmented negative-sense RNA viruses (nsNSVs)—including highly pathogenic pathogens such as measles virus (MeV), Nipah virus (NiV), Hendra virus (HeV), Ebola virus (EBOV), and others—pose major global health threats, yet most lack approved antiviral therapeutics. In the recent study, high-resolution cryo-electron microscopy (cryo-EM) revealed previously unrecognized allosteric pockets in the large (L) polymerase proteins of MeV and NiV, spatially distinct from the catalytic nucleotide-binding site. We further demonstrated that the non-nucleoside inhibitor ERDRP-0519 engages these pockets to allosterically ‘lock’ the polymerase in a mechanically inactive state. These findings reveal an allosteric mechanism of inhibition rooted in the conformational mechanics of the enzyme and highlight opportunities for integrating artificial intelligence (AI)-aided drug discovery (AIDD) into rational drug design.</div></div>","PeriodicalId":100900,"journal":{"name":"Mechanobiology in Medicine","volume":"3 4","pages":"Article 100156"},"PeriodicalIF":0.0,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145009942","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 : 2025-12-01Epub Date: 2025-09-24DOI: 10.1016/j.mbm.2025.100158
Mirko D'Urso , Pim van den Bersselaar , Sarah Pragnere , Paolo Maiuri , Carlijn V.C. Bouten , Nicholas A. Kurniawan
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-β-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.
{"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":"2025-12-01","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}
Pub Date : 2025-12-01Epub Date: 2025-10-21DOI: 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 : 2025-12-01Epub 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":"2025-12-01","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 : 2025-12-01Epub 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":"2025-12-01","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}
Pub Date : 2025-12-01Epub 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":"2025-12-01","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 : 2025-12-01Epub 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":"2025-12-01","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 : 2025-09-01Epub Date: 2025-08-16DOI: 10.1016/j.mbm.2025.100147
Yunlong Huo
Diffuse myocardial fibrosis affects disease severity and outcomes in multiple heart diseases. A recent study in NATURE has shown a chemomechanical method to regulate myocardial stromal cell states to suppress fibrosis in vitro and in vivo, which provides a proof-of-concept therapeutic strategy. This study reviews the proposed chemomechanical method and other recent biotechnologies to fight cardiac fibrosis.
{"title":"Fighting cardiac fibrosis using the chemomechanical method","authors":"Yunlong Huo","doi":"10.1016/j.mbm.2025.100147","DOIUrl":"10.1016/j.mbm.2025.100147","url":null,"abstract":"<div><div>Diffuse myocardial fibrosis affects disease severity and outcomes in multiple heart diseases. A recent study in NATURE has shown a chemomechanical method to regulate myocardial stromal cell states to suppress fibrosis in vitro and in vivo, which provides a proof-of-concept therapeutic strategy. This study reviews the proposed chemomechanical method and other recent biotechnologies to fight cardiac fibrosis.</div></div>","PeriodicalId":100900,"journal":{"name":"Mechanobiology in Medicine","volume":"3 3","pages":"Article 100147"},"PeriodicalIF":0.0,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144863143","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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