Pub Date : 2026-03-01Epub 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":"2026-03-01","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 : 2026-03-01Epub Date: 2026-03-04DOI: 10.1016/j.mbm.2026.100178
Jiacheng Lei , Yicen Long , Xiaojing Liu , Zhiqin Chu , Qiang Wei
Stress fiber–generated traction forces critically regulate mesenchymal stem cell (MSC) behavior, yet how mechanical cues are integrated across transcriptional programs remains unclear. Here, we attenuated actomyosin contractility in human MSCs and performed parallel Assay for Transposase-Accessible Chromatin with high-throughput sequencing (ATAC-seq), YAP-targeted Cleavage Under Targets and Tagmentation sequencing (CUT&Tag) and RNA-seq profiling. We show that reduced stress fiber traction force selectively reorganizes chromatin accessibility into coherent functional modules, resulting in diverse transcriptional programs. The mechanosensitive co-activator YAP functions as a parallel force-responsive regulatory layer coordinating with chromatin accessibility changes. Integration of chromatin accessibility, YAP occupancy, and transcriptomic profiles reveals pathway-specific regulatory responses, identifying focal adhesion and PI3K-Akt signaling as central mechanosensitive pathways coordinated across layers. Together, these findings establish a modular framework for force-dependent gene regulation, demonstrating how mechanical signals are integrated across epigenomic and transcriptional networks to shape MSC transcriptional programs.
{"title":"Stress fiber traction force reshapes chromatin accessibility and YAP binding to direct diverse transcriptional programs in mesenchymal stem cells","authors":"Jiacheng Lei , Yicen Long , Xiaojing Liu , Zhiqin Chu , Qiang Wei","doi":"10.1016/j.mbm.2026.100178","DOIUrl":"10.1016/j.mbm.2026.100178","url":null,"abstract":"<div><div>Stress fiber–generated traction forces critically regulate mesenchymal stem cell (MSC) behavior, yet how mechanical cues are integrated across transcriptional programs remains unclear. Here, we attenuated actomyosin contractility in human MSCs and performed parallel Assay for Transposase-Accessible Chromatin with high-throughput sequencing (ATAC-seq), YAP-targeted Cleavage Under Targets and Tagmentation sequencing (CUT&Tag) and RNA-seq profiling. We show that reduced stress fiber traction force selectively reorganizes chromatin accessibility into coherent functional modules, resulting in diverse transcriptional programs. The mechanosensitive co-activator YAP functions as a parallel force-responsive regulatory layer coordinating with chromatin accessibility changes. Integration of chromatin accessibility, YAP occupancy, and transcriptomic profiles reveals pathway-specific regulatory responses, identifying focal adhesion and PI3K-Akt signaling as central mechanosensitive pathways coordinated across layers. Together, these findings establish a modular framework for force-dependent gene regulation, demonstrating how mechanical signals are integrated across epigenomic and transcriptional networks to shape MSC transcriptional programs.</div></div>","PeriodicalId":100900,"journal":{"name":"Mechanobiology in Medicine","volume":"4 1","pages":"Article 100178"},"PeriodicalIF":0.0,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147396141","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 : 2026-03-01Epub Date: 2026-03-03DOI: 10.1016/j.mbm.2026.100179
Fazlur Rashid , Ning Wang
Over the last few decades, physical principles have been proposed to explain some biological processes and functions. However, biological principles remain elusive. A biological principle is a governing rule that guides the structure and functions of cells. Biological principles are built upon the laws of physics and chemistry, but they go beyond these laws and are unique to living matter. Here, we discuss what differentiates a biological principle from a physical principle and discuss candidates for biological principles. We review evidence from literature that regulation of cytoskeletal prestress (endogenous cytoskeletal pre-existing tensile stress) is essential for governing biological structures and functions of living cells. We propose that, in addition to the biological principles of Central Dogma and metabolism, cytoskeletal prestress homeostasis is a biological principle of a living cell across all domains of life. We propose that living cells regulate their stress and modulus to limit maximum strain on the cells. Homeostasis of endogenous energy-dependent, stress-supported systems that use cytoskeletal (CSK) prestress (the force of life) to stabilize structure represents a biological principle of a living cell that is not observed in inorganic systems, whereas other basic principles (e.g., self-assembly) are required for living systems but are also found in simpler nonliving systems. Leveraging biological principles of cells may have far-reaching implications in understanding the essence of cell life and designing effective interventions for therapeutics to advance medicine and enhance human health.
{"title":"Cytoskeletal prestress homeostasis is a biological principle that governs living cell structure and function","authors":"Fazlur Rashid , Ning Wang","doi":"10.1016/j.mbm.2026.100179","DOIUrl":"10.1016/j.mbm.2026.100179","url":null,"abstract":"<div><div>Over the last few decades, physical principles have been proposed to explain some biological processes and functions. However, biological principles remain elusive. A biological principle is a governing rule that guides the structure and functions of cells. Biological principles are built upon the laws of physics and chemistry, but they go beyond these laws and are unique to living matter. Here, we discuss what differentiates a biological principle from a physical principle and discuss candidates for biological principles. We review evidence from literature that regulation of cytoskeletal prestress (endogenous cytoskeletal pre-existing tensile stress) is essential for governing biological structures and functions of living cells. We propose that, in addition to the biological principles of Central Dogma and metabolism, cytoskeletal prestress homeostasis is a biological principle of a living cell across all domains of life. We propose that living cells regulate their stress and modulus to limit maximum strain on the cells. Homeostasis of endogenous energy-dependent, stress-supported systems that use cytoskeletal (CSK) prestress (the force of life) to stabilize structure represents a biological principle of a living cell that is not observed in inorganic systems, whereas other basic principles (e.g., self-assembly) are required for living systems but are also found in simpler nonliving systems. Leveraging biological principles of cells may have far-reaching implications in understanding the essence of cell life and designing effective interventions for therapeutics to advance medicine and enhance human health.</div></div>","PeriodicalId":100900,"journal":{"name":"Mechanobiology in Medicine","volume":"4 1","pages":"Article 100179"},"PeriodicalIF":0.0,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147448810","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 : 2026-03-01Epub 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":"2026-03-01","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 : 2026-03-01Epub 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":"2026-03-01","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 : 2026-03-01Epub Date: 2026-02-24DOI: 10.1016/j.mbm.2026.100177
Xiangcheng Chen , Maximilian Wang , Ning Jiang
T cells are traditionally viewed as non-phagocytic lymphocytes that recognize antigens via the T cell receptor (TCR) and mediate cytotoxicity at the immunological synapse, while phagocytosis is performed by professional phagocytes such as macrophages and dendritic cells. Here we show that peptide–MHC (pMHC) recognition alone is sufficient to drive rapid, antigen-specific phagocytosis by Jurkat T cells. We generated CD8+ Jurkat cells expressing a class I–restricted human TCR (SVAR16) with intermediate-to-high 2-dimensional (2D) affinity for the SARS-CoV-2 epitope HLA∗A2:01–YLQ and used a micropipette system to control and image T cell interaction with pMHC coated beads. Upon contact with cognate YLQ-coated beads, SVAR16 transduced CD8+ Jurkat cells consistently formed phagosomes within minutes and completely internalized beads with consistent kinetics. These results demonstrate that appropriately tuned TCR–pMHC interactions, supported by CD8 co-receptors, can convert a canonical CD4+ T cell line into an antigen-specific phagocyte. This work reports a novel effector function of T cells and suggests that TCR-engineering could convert CD4+ T cells into phagocytes, potentially revealing a new approach to T cell-based cancer immunotherapy.
{"title":"TCR-pMHC recognition mediates target phagocytosis by T cells","authors":"Xiangcheng Chen , Maximilian Wang , Ning Jiang","doi":"10.1016/j.mbm.2026.100177","DOIUrl":"10.1016/j.mbm.2026.100177","url":null,"abstract":"<div><div>T cells are traditionally viewed as non-phagocytic lymphocytes that recognize antigens via the T cell receptor (TCR) and mediate cytotoxicity at the immunological synapse, while phagocytosis is performed by professional phagocytes such as macrophages and dendritic cells. Here we show that peptide–MHC (pMHC) recognition alone is sufficient to drive rapid, antigen-specific phagocytosis by Jurkat T cells. We generated CD8<sup>+</sup> Jurkat cells expressing a class I–restricted human TCR (SVAR16) with intermediate-to-high 2-dimensional (2D) affinity for the SARS-CoV-2 epitope HLA∗A2:01–YLQ and used a micropipette system to control and image T cell interaction with pMHC coated beads. Upon contact with cognate YLQ-coated beads, SVAR16 transduced CD8<sup>+</sup> Jurkat cells consistently formed phagosomes within minutes and completely internalized beads with consistent kinetics. These results demonstrate that appropriately tuned TCR–pMHC interactions, supported by CD8 co-receptors, can convert a canonical CD4<sup>+</sup> T cell line into an antigen-specific phagocyte. This work reports a novel effector function of T cells and suggests that TCR-engineering could convert CD4<sup>+</sup> T cells into phagocytes, potentially revealing a new approach to T cell-based cancer immunotherapy.</div></div>","PeriodicalId":100900,"journal":{"name":"Mechanobiology in Medicine","volume":"4 1","pages":"Article 100177"},"PeriodicalIF":0.0,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147396140","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 : 2026-03-01Epub Date: 2026-02-24DOI: 10.1016/j.mbm.2026.100176
Ran Xu , Xu Jiang , Yushun Tao , Shikun Fang , Jie Li , Fan Zhao , Fujun Wang , Liao Wang , Jun Zhang
Knee osteoarthritis (KOA) is fundamentally driven by abnormal mechanical loading and the subsequent loss of joint homeostasis. Effective therapeutic strategies, whether conservative or surgical, depend on the precise restoration of physiological kinematics and load distribution. This review synthesizes recent advances in sensor technologies designed to quantify the mechanobiological environment of the knee. In non-surgical management, wearable systems utilizing inertial measurement units (IMU) and flexible pressure sensors enable the continuous monitoring of gait cycles, joint angles, and muscle activation, providing objective data for neuromuscular rehabilitation. In surgical contexts, we analyze the evolution of intraoperative sensing from rigid force-sensing spacers to emerging soft electronics in total knee arthroplasty (TKA). A critical challenge remains in developing sensors with mechanical compliance similar to biological tissues and minimal thickness to fit the constrained joint space during joint-preserving procedures. We highlight the potential of novel transduction mechanisms—including piezoresistive, capacitive, piezoelectric, and triboelectric systems—to overcome these limitations. The integration of these flexible, self-powered technologies with data-driven analytics offers a pathway toward an integrated data-driven treatment framework, which could facilitate optimal biomechanical alignment and functional recovery.
{"title":"Portable electronic devices for mechanotherapy and operative treatment of osteoarthritis","authors":"Ran Xu , Xu Jiang , Yushun Tao , Shikun Fang , Jie Li , Fan Zhao , Fujun Wang , Liao Wang , Jun Zhang","doi":"10.1016/j.mbm.2026.100176","DOIUrl":"10.1016/j.mbm.2026.100176","url":null,"abstract":"<div><div>Knee osteoarthritis (KOA) is fundamentally driven by abnormal mechanical loading and the subsequent loss of joint homeostasis. Effective therapeutic strategies, whether conservative or surgical, depend on the precise restoration of physiological kinematics and load distribution. This review synthesizes recent advances in sensor technologies designed to quantify the mechanobiological environment of the knee. In non-surgical management, wearable systems utilizing inertial measurement units (IMU) and flexible pressure sensors enable the continuous monitoring of gait cycles, joint angles, and muscle activation, providing objective data for neuromuscular rehabilitation. In surgical contexts, we analyze the evolution of intraoperative sensing from rigid force-sensing spacers to emerging soft electronics in total knee arthroplasty (TKA). A critical challenge remains in developing sensors with mechanical compliance similar to biological tissues and minimal thickness to fit the constrained joint space during joint-preserving procedures. We highlight the potential of novel transduction mechanisms—including piezoresistive, capacitive, piezoelectric, and triboelectric systems—to overcome these limitations. The integration of these flexible, self-powered technologies with data-driven analytics offers a pathway toward an integrated data-driven treatment framework, which could facilitate optimal biomechanical alignment and functional recovery.</div></div>","PeriodicalId":100900,"journal":{"name":"Mechanobiology in Medicine","volume":"4 1","pages":"Article 100176"},"PeriodicalIF":0.0,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147396142","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 : 2026-03-01Epub Date: 2026-02-18DOI: 10.1016/j.mbm.2026.100175
Yiming Han , Xiaocen Duan , Shuyi Wang , Shuqiang Huang , Kui Zhu , Jianyong Huang
Mechanical microenvironments are increasingly recognized as a key regulator of host-pathogen interactions. External mechanical stimuli, including shear stress, cyclic stretch, and hydrostatic pressure, strongly modulate bacterial adhesion and invasion. Yet, how mechanobiological cues in tissue microenvironments shape bacterial pathogenesis is still poorly understood. In a recent study, Han and colleagues demonstrate that a variety of pathogens exploit mechanobiological cues in tissue microenvironments to facilitate infections. These findings identify cellular mechanics as a pivotal and underappreciated determinant during bacterial infections and shed light on the discovery and development of alternative mechanobiology-driven antimicrobial strategies.
{"title":"Pathogen-host infection modulated by mechanobiological cues in tissue microenvironments","authors":"Yiming Han , Xiaocen Duan , Shuyi Wang , Shuqiang Huang , Kui Zhu , Jianyong Huang","doi":"10.1016/j.mbm.2026.100175","DOIUrl":"10.1016/j.mbm.2026.100175","url":null,"abstract":"<div><div>Mechanical microenvironments are increasingly recognized as a key regulator of host-pathogen interactions. External mechanical stimuli, including shear stress, cyclic stretch, and hydrostatic pressure, strongly modulate bacterial adhesion and invasion. Yet, how mechanobiological cues in tissue microenvironments shape bacterial pathogenesis is still poorly understood. In a recent study, Han and colleagues demonstrate that a variety of pathogens exploit mechanobiological cues in tissue microenvironments to facilitate infections. These findings identify cellular mechanics as a pivotal and underappreciated determinant during bacterial infections and shed light on the discovery and development of alternative mechanobiology-driven antimicrobial strategies.</div></div>","PeriodicalId":100900,"journal":{"name":"Mechanobiology in Medicine","volume":"4 1","pages":"Article 100175"},"PeriodicalIF":0.0,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147380157","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 : 2026-03-01Epub 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":"2026-03-01","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}
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.
{"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":"2025-12-01","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}
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