Pub Date : 2026-02-07DOI: 10.1016/j.bmt.2026.100135
Chaojin Li , Feng Gong , Xiaodong Liu , Ang Li
Currently, nanoparticles (NPs) still face challenges in achieving efficient tumor targeted delivery, especially in balancing in vivo distribution and cellular uptake efficiency. A recent study published in Advanced Functional Materials utilized DNA barcoding combined with high-throughput in vivo screening to systematically evaluate the targeting of gold NPs of different shapes and sizes in tumors. The results showed that large-sized triangular gold NPs exhibited the highest cellular uptake efficiency in vitro, and achieved significant tumor enrichment and excellent siRNA delivery in vivo through surface modification of RGD peptides. Further photothermal experiments showed that triangular particles can rapidly raise the temperature to 57 °C in the tumor area, achieving effective tumor ablation. This study indicates that large triangular gold NPs possess advantages in cellular uptake, in vivo enrichment ability, and photothermal therapy potential, providing a new strategy for precise tumor targeted therapy. The study highlights that nanoparticle morphology plays a dominant role in governing in vivo tumor accumulation and therapeutic outcomes.
{"title":"Barcode screening reveals the key role of gold nanoparticle morphology in tumor targeting","authors":"Chaojin Li , Feng Gong , Xiaodong Liu , Ang Li","doi":"10.1016/j.bmt.2026.100135","DOIUrl":"10.1016/j.bmt.2026.100135","url":null,"abstract":"<div><div>Currently, nanoparticles (NPs) still face challenges in achieving efficient tumor targeted delivery, especially in balancing in vivo distribution and cellular uptake efficiency. A recent study published in Advanced Functional Materials utilized DNA barcoding combined with high-throughput in vivo screening to systematically evaluate the targeting of gold NPs of different shapes and sizes in tumors. The results showed that large-sized triangular gold NPs exhibited the highest cellular uptake efficiency in vitro, and achieved significant tumor enrichment and excellent siRNA delivery in vivo through surface modification of RGD peptides. Further photothermal experiments showed that triangular particles can rapidly raise the temperature to 57 °C in the tumor area, achieving effective tumor ablation. This study indicates that large triangular gold NPs possess advantages in cellular uptake, in vivo enrichment ability, and photothermal therapy potential, providing a new strategy for precise tumor targeted therapy. The study highlights that nanoparticle morphology plays a dominant role in governing in vivo tumor accumulation and therapeutic outcomes.</div></div>","PeriodicalId":100180,"journal":{"name":"Biomedical Technology","volume":"13 ","pages":"Article 100135"},"PeriodicalIF":0.0,"publicationDate":"2026-02-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146173763","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 : 2026-02-04DOI: 10.1016/j.bmt.2026.100134
Junwei Xu , Yi Cui , Xuemei Sun , Zhiheng Chen , Kun Li , Meili Liu , Ping Li
Background
Osteochondral defects pose significant clinical challenges owing to the complex anisotropic collagen alignment of osteochondral tissue and its limited self-healing capacity. Although mechanically biomimetic scaffolds have been widely applied in osteochondral repair, existing scaffolds exhibit limited structural and functional biomimicry, resulting in osteochondral repair efficacy that requires further improvement.
Technology
Bioinspired by the unique collagen fiber alignment of natural osteochondral tissue, this study developed a technology of magnetically guided ordered biphasic scaffold combined with gradient magnetic field stimulation. Via alkaline dissolution and thermal crosslinking, Fe3O4 nanochains (NCs) were horizontally oriented in the agarose-based cartilage phase and vertically oriented in the poly(ethylene glycol) diacrylate/agarose-based subchondral bone phase. This scaffold system synergized with a 3–15 mT gradient magnetic field (MF) to enable the integrated repair of osteochondral defects.
Results
We adjusted the scaffold's magnetism by modulating the content of Fe3O4 NCs, and further investigated the impacts of the magnetic ordered scaffolds and external MF on the differentiation of bone marrow mesenchymal stem cells. Results showed that the cartilage-phase scaffold (0.025 % w/v NCs, 0.27 emu/g) upregulated type II collagen (chondrogenesis), while the subchondral bone-phase scaffold (1.0 % w/v NCs, 1.20 emu/g) boosted osteogenic differentiation. Specifically, 3 mT static MF enhanced chondrogenesis via ECM-receptor signaling, while 15 mT static MF stimulated osteogenesis by activating PI3K/Akt pathway. Animal studies demonstrated that the magnetic biphasic hierarchical scaffold combined with 3–15 mT gradient MF significantly improved osteochondral repair, including nearly double the new subchondral bone volume fraction, a smoother cartilage surface, and collagen fiber alignment that more closely resembled natural osteochondral tissue. This work highlights the potential of the magnetic ordered scaffold-gradient MF technology in osteochondral repair, and is further poised for synergistic development with 3D bioprinting, intelligent manufacturing, and single-cell sequencing, injecting new impetus into the clinical translation of magnetic tissue engineering.
{"title":"Integrated strategy of collagen fiber arrangement-inspired magnetic nanochain-doped ordered biphasic scaffold and gradient magnetic field stimulation for osteochondral regeneration","authors":"Junwei Xu , Yi Cui , Xuemei Sun , Zhiheng Chen , Kun Li , Meili Liu , Ping Li","doi":"10.1016/j.bmt.2026.100134","DOIUrl":"10.1016/j.bmt.2026.100134","url":null,"abstract":"<div><h3>Background</h3><div>Osteochondral defects pose significant clinical challenges owing to the complex anisotropic collagen alignment of osteochondral tissue and its limited self-healing capacity. Although mechanically biomimetic scaffolds have been widely applied in osteochondral repair, existing scaffolds exhibit limited structural and functional biomimicry, resulting in osteochondral repair efficacy that requires further improvement.</div></div><div><h3>Technology</h3><div>Bioinspired by the unique collagen fiber alignment of natural osteochondral tissue, this study developed a technology of magnetically guided ordered biphasic scaffold combined with gradient magnetic field stimulation. Via alkaline dissolution and thermal crosslinking, Fe<sub>3</sub>O<sub>4</sub> nanochains (NCs) were horizontally oriented in the agarose-based cartilage phase and vertically oriented in the poly(ethylene glycol) diacrylate/agarose-based subchondral bone phase. This scaffold system synergized with a 3–15 mT gradient magnetic field (MF) to enable the integrated repair of osteochondral defects.</div></div><div><h3>Results</h3><div>We adjusted the scaffold's magnetism by modulating the content of Fe<sub>3</sub>O<sub>4</sub> NCs, and further investigated the impacts of the magnetic ordered scaffolds and external MF on the differentiation of bone marrow mesenchymal stem cells. Results showed that the cartilage-phase scaffold (0.025 % w/v NCs, 0.27 emu/g) upregulated type II collagen (chondrogenesis), while the subchondral bone-phase scaffold (1.0 % w/v NCs, 1.20 emu/g) boosted osteogenic differentiation. Specifically, 3 mT static MF enhanced chondrogenesis via ECM-receptor signaling, while 15 mT static MF stimulated osteogenesis by activating PI3K/Akt pathway. Animal studies demonstrated that the magnetic biphasic hierarchical scaffold combined with 3–15 mT gradient MF significantly improved osteochondral repair, including nearly double the new subchondral bone volume fraction, a smoother cartilage surface, and collagen fiber alignment that more closely resembled natural osteochondral tissue. This work highlights the potential of the magnetic ordered scaffold-gradient MF technology in osteochondral repair, and is further poised for synergistic development with 3D bioprinting, intelligent manufacturing, and single-cell sequencing, injecting new impetus into the clinical translation of magnetic tissue engineering.</div></div>","PeriodicalId":100180,"journal":{"name":"Biomedical Technology","volume":"13 ","pages":"Article 100134"},"PeriodicalIF":0.0,"publicationDate":"2026-02-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146173671","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}
Tardigrades have attracted widespread research attention due to their extraordinary radiotolerance, of which the damage suppressor protein (DSUP) is regarded as a key molecule responsible for their robust DNA repair capability. How to translate these findings into safe and efficacious radioprotection strategies for humans remains an ongoing research challenge.
Technology
Given that ionizing radiation (IR)-induced hematopoietic failure caused by depletion of bone marrow hematopoietic stem/progenitor cells (HSPCs) is a major cause of mortality, we propose using gene editing and stem cell technologies to precisely knock in DSUP gene into isolated murine HSPCs, thereby generating HSPCs with enhanced radiotolerance. In this study, we first obtained DSUP-modified mouse HSPCs by isolating, culturing, and transfecting mouse HSPCs using lentivirus transfection, as well as DSUP-modified human HSPCs via three stages of hematopoietic induction and differentiation from DSUP-modified human pluripotent stem cells (PSCs).
Results
The radioprotection capacity of DSUP-modified stem cells was confirmed by a series of in vitro assays. Given the differentiation potential of myeloid progenitor cells (MPCs) and without requirement for human leukocyte antigen matching during hematopoietic stem cell transplant, we then obtained DSUP-modified mouse MPCs by differentiated from the expanded mouse HSPCs in polyvinyl alcohol (PVA) culture system for more than 30 days. DSUP-modified MPCs can also maintain lower radiation-induced apoptosis and DNA damage. Pre-infusion of DSUP-modified MPCs improves irradiated-mice survival rate by 30 % without long-term side effects. While not residing in bone marrow or spleen, these cells alleviated hematopoietic failure by restoring peripheral red blood cells and platelets and accelerated hematopoietic recovery. Mechanistically, DSUP forms phase separation structures that can recruit DNA repair proteins to double-strand breaks, promoting homologous recombination repair. Taken together, our results demonstrated DSUP-modified MPCs offer a promising stem cell-based radioprotection technology, highlighting a novel biomimetic approach for radioprotection.
{"title":"Integrated tardigrade-based biomimetic strategy and stem cell expansion and differentiation for a novel radioprotection approach","authors":"Biao Zhang , Jun-Nian Zhou , Quan Zeng , Zhi-Rui Liu, Yu-Ting Gao, Fu-Dong Chen, Tao Fan, Ya-Li Jia, Jia-Fei Xi, Xue-Tao Pei, Wen Yue","doi":"10.1016/j.bmt.2025.100132","DOIUrl":"10.1016/j.bmt.2025.100132","url":null,"abstract":"<div><h3>Background</h3><div>Tardigrades have attracted widespread research attention due to their extraordinary radiotolerance, of which the damage suppressor protein (DSUP) is regarded as a key molecule responsible for their robust DNA repair capability. How to translate these findings into safe and efficacious radioprotection strategies for humans remains an ongoing research challenge.</div></div><div><h3>Technology</h3><div>Given that ionizing radiation (IR)-induced hematopoietic failure caused by depletion of bone marrow hematopoietic stem/progenitor cells (HSPCs) is a major cause of mortality, we propose using gene editing and stem cell technologies to precisely knock in DSUP gene into isolated murine HSPCs, thereby generating HSPCs with enhanced radiotolerance. In this study, we first obtained DSUP-modified mouse HSPCs by isolating, culturing, and transfecting mouse HSPCs using lentivirus transfection, as well as DSUP-modified human HSPCs via three stages of hematopoietic induction and differentiation from DSUP-modified human pluripotent stem cells (PSCs).</div></div><div><h3>Results</h3><div>The radioprotection capacity of <em>DSUP</em>-modified stem cells was confirmed by a series of <em>in vitro</em> assays. Given the differentiation potential of myeloid progenitor cells (MPCs) and without requirement for human leukocyte antigen matching during hematopoietic stem cell transplant, we then obtained <em>DSUP</em>-modified mouse MPCs by differentiated from the expanded mouse HSPCs in polyvinyl alcohol (PVA) culture system for more than 30 days. <em>DSUP</em>-modified MPCs can also maintain lower radiation-induced apoptosis and DNA damage. Pre-infusion of <em>DSUP</em>-modified MPCs improves irradiated-mice survival rate by 30 % without long-term side effects. While not residing in bone marrow or spleen, these cells alleviated hematopoietic failure by restoring peripheral red blood cells and platelets and accelerated hematopoietic recovery. Mechanistically, DSUP forms phase separation structures that can recruit DNA repair proteins to double-strand breaks, promoting homologous recombination repair. Taken together, our results demonstrated <em>DSUP</em>-modified MPCs offer a promising stem cell-based radioprotection technology, highlighting a novel biomimetic approach for radioprotection.</div></div>","PeriodicalId":100180,"journal":{"name":"Biomedical Technology","volume":"13 ","pages":"Article 100132"},"PeriodicalIF":0.0,"publicationDate":"2026-01-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146079319","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 : 2026-01-08DOI: 10.1016/j.bmt.2025.100131
Zhe Wang , Xiang Lin , Yunpeng Shi , Hong Yan , Yixuan Shang , Haozhen Ren
Background
In recent years, tissue engineering has experienced rapid development, with bioscaffolds emerging as a focal point of research due to their favorable bioactivity, biocompatibility, and capacity to provide mechanical support for cellular growth. The bioscaffolds have great potential in tissue regeneration. However, conventional natural scaffolds and polymer scaffolds pose risks of immunogenicity, while also face challenges in mimicking the in vivo microenvironment and the biochemical and mechanical properties of natural organs/tissues, which collectively limit their repair capability. The development of decellularized extracellular matrix (dECM) technology offers a viable solution to these challenges, demonstrating considerable potential for advancing organ and tissue regeneration.
Technology
This reviews the classification of dECM, outlines various current methods for its preparation, and comprehensively examines its latest advances in tissue repair and regenerative medicine, including applications in skin, bone, nerve, heart, lung, liver, and kidney tissues.
Results
This review systematically examines recent advances in dECM production and regenerative medicine applications. We classify dECM subtypes, detail contemporary decellularization protocols, and highlight their biomedical utility. Superior biocompatibility substantially mitigates post-transplant immune rejection risk, underscoring strong clinical translation potential for tissue engineering.
{"title":"Decellularized extracellular matrix: Advanced bioplatforms for functional tissue restoration via innovative decellularization techniques","authors":"Zhe Wang , Xiang Lin , Yunpeng Shi , Hong Yan , Yixuan Shang , Haozhen Ren","doi":"10.1016/j.bmt.2025.100131","DOIUrl":"10.1016/j.bmt.2025.100131","url":null,"abstract":"<div><h3>Background</h3><div>In recent years, tissue engineering has experienced rapid development, with bioscaffolds emerging as a focal point of research due to their favorable bioactivity, biocompatibility, and capacity to provide mechanical support for cellular growth. The bioscaffolds have great potential in tissue regeneration. However, conventional natural scaffolds and polymer scaffolds pose risks of immunogenicity, while also face challenges in mimicking the <em>in vivo</em> microenvironment and the biochemical and mechanical properties of natural organs/tissues, which collectively limit their repair capability. The development of decellularized extracellular matrix (dECM) technology offers a viable solution to these challenges, demonstrating considerable potential for advancing organ and tissue regeneration.</div></div><div><h3>Technology</h3><div>This reviews the classification of dECM, outlines various current methods for its preparation, and comprehensively examines its latest advances in tissue repair and regenerative medicine, including applications in skin, bone, nerve, heart, lung, liver, and kidney tissues.</div></div><div><h3>Results</h3><div>This review systematically examines recent advances in dECM production and regenerative medicine applications. We classify dECM subtypes, detail contemporary decellularization protocols, and highlight their biomedical utility. Superior biocompatibility substantially mitigates post-transplant immune rejection risk, underscoring strong clinical translation potential for tissue engineering.</div></div>","PeriodicalId":100180,"journal":{"name":"Biomedical Technology","volume":"13 ","pages":"Article 100131"},"PeriodicalIF":0.0,"publicationDate":"2026-01-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145915116","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}
<div><div>Fracture healing remains a significant clinical challenge, particularly in cases of delayed or impaired recovery, often hindered by inadequate vascularization, patient variability. Conventional stimulation methods relying on implanted electrodes or external coils are constrained by invasiveness, complexity, and patient discomfort. Smart biomaterials capable of providing wireless, localized bioelectric stimulation represent a promising alternative. Among these, magnetoelectric (ME) laminates can convert externally applied magnetic fields into localized therapeutic voltages, enabling non-invasive and patient-specific bone regeneration. Although magnetoelectric systems have shown potential in biomedical stimulation, their electromechanical coupling behavior, tunability, and optimization for orthopedic applications remain insufficiently explored. Understanding these mechanisms through computational modeling is crucial for developing clinically translatable ME-based bone regeneration systems. This study introduces a next-generation trilayer ME laminate integrating a new material pairing: magnetostrictive Galfenol (Fe<sub>80</sub>Ga<sub>20</sub>) with a piezoelectric layer of either poly(vinylidene fluoride)(PVDF) or Barium Titanate (BaTiO<sub>3</sub>). A fully coupled 3D finite-element model was developed in COMSOL Multiphysics 6.0 to simulate magnetostrictive deformation, interfacial strain transfer, and piezoelectric voltage generation under physiologically relevant magnetic field strengths and frequencies. Parametric studies assessed tunability across varying excitation conditions, while comparative analyses evaluated the performance trade-offs between PVDF- and BaTiO<sub>3</sub>-based laminates. Simulations revealed that the proposed trilayer laminate could generate sustained voltage outputs within the osteogenesis-relevant range (100 nV–5 V) without implanted electrodes. Resonance-dependent voltage peaks were sensitive to excitation frequency and adaptable to bone geometry, supporting personalized stimulation protocols. PVDF-based laminates provided higher flexibility and biocompatibility, whereas BaTiO<sub>3</sub>-based laminates achieved superior voltage outputs, highlighting design trade-offs relevant for clinical optimization. This work establishes the engineering feasibility and fundamental electromechanical characteristics of magnetoelectric trilayer laminates for wireless bone stimulation. The deterministic modeling approach, incorporating parameter sweeps for laminate thickness, field amplitude, and excitation frequency, provides a first-level sensitivity framework for device design. Overall, the study bridges computational modeling and translational potential, positioning ME laminates as a next-generation platform for non-invasive, customizable, and patient-centered bone regeneration. These findings lay the groundwork for forthcoming <em>in-vitro</em> and <em>in-vivo</em> validations, advancing the integration of smart magnetoe
{"title":"Wireless bioelectric stimulation for bone regeneration using magnetoelectric PVDF/BaTiO3 – Fe80Ga20 laminates","authors":"H.A. Viraji , Aravinda Abeygunawardane , S.U. Adikary , Sajith Edirisinghe , Aadil Faleel","doi":"10.1016/j.bmt.2025.100121","DOIUrl":"10.1016/j.bmt.2025.100121","url":null,"abstract":"<div><div>Fracture healing remains a significant clinical challenge, particularly in cases of delayed or impaired recovery, often hindered by inadequate vascularization, patient variability. Conventional stimulation methods relying on implanted electrodes or external coils are constrained by invasiveness, complexity, and patient discomfort. Smart biomaterials capable of providing wireless, localized bioelectric stimulation represent a promising alternative. Among these, magnetoelectric (ME) laminates can convert externally applied magnetic fields into localized therapeutic voltages, enabling non-invasive and patient-specific bone regeneration. Although magnetoelectric systems have shown potential in biomedical stimulation, their electromechanical coupling behavior, tunability, and optimization for orthopedic applications remain insufficiently explored. Understanding these mechanisms through computational modeling is crucial for developing clinically translatable ME-based bone regeneration systems. This study introduces a next-generation trilayer ME laminate integrating a new material pairing: magnetostrictive Galfenol (Fe<sub>80</sub>Ga<sub>20</sub>) with a piezoelectric layer of either poly(vinylidene fluoride)(PVDF) or Barium Titanate (BaTiO<sub>3</sub>). A fully coupled 3D finite-element model was developed in COMSOL Multiphysics 6.0 to simulate magnetostrictive deformation, interfacial strain transfer, and piezoelectric voltage generation under physiologically relevant magnetic field strengths and frequencies. Parametric studies assessed tunability across varying excitation conditions, while comparative analyses evaluated the performance trade-offs between PVDF- and BaTiO<sub>3</sub>-based laminates. Simulations revealed that the proposed trilayer laminate could generate sustained voltage outputs within the osteogenesis-relevant range (100 nV–5 V) without implanted electrodes. Resonance-dependent voltage peaks were sensitive to excitation frequency and adaptable to bone geometry, supporting personalized stimulation protocols. PVDF-based laminates provided higher flexibility and biocompatibility, whereas BaTiO<sub>3</sub>-based laminates achieved superior voltage outputs, highlighting design trade-offs relevant for clinical optimization. This work establishes the engineering feasibility and fundamental electromechanical characteristics of magnetoelectric trilayer laminates for wireless bone stimulation. The deterministic modeling approach, incorporating parameter sweeps for laminate thickness, field amplitude, and excitation frequency, provides a first-level sensitivity framework for device design. Overall, the study bridges computational modeling and translational potential, positioning ME laminates as a next-generation platform for non-invasive, customizable, and patient-centered bone regeneration. These findings lay the groundwork for forthcoming <em>in-vitro</em> and <em>in-vivo</em> validations, advancing the integration of smart magnetoe","PeriodicalId":100180,"journal":{"name":"Biomedical Technology","volume":"12 ","pages":"Article 100121"},"PeriodicalIF":0.0,"publicationDate":"2025-11-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145578954","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 : 2025-11-19DOI: 10.1016/j.bmt.2025.100120
Zixuan Tang , Qingquan Xia , Jian Li , Jun Chen , Xuhua Wu , Jiang Li , Jiangyi Liu , Wei Liu , Ke Rong , Xiangchao Meng
The healing of acute infected wounds is a multi-stage and sequential biological process. Traditional antibacterial dressings are usually a simple superposition of antibacterial properties and active ingredients, lacking effective coupling with the wound microenvironment, and it is difficult to accurately match the continuous process of infected wound healing. In this study, a pH-responsive hydrogel of sodium alginate and carboxymethyl chitosan interpenetrating network was constructed, and tannic acid (TA) and zinc-doped bioglass (BAG) were loaded through hydrogen bonding and hydrophobic interactions. In the acidic environment of infection, the enhancement of intermolecular non-covalent interaction leads to the contraction of hydrogel network and the rapid release of TA. In the alkaline environment of healing, the weakening of intermolecular interaction leads to the expansion of hydrogel network and the continuous release of Zn2+ and Ca2+. In vitro biological evaluation showed that the hydrogel had an effective antibacterial effects against E.coli and S.aureus, and effectively regulated immune response. In addition, the hydrogel effectively removed excessive ROS and significantly increase the activity of cellular antioxidant enzymes, thereby accelerating the wound healing process in animal experiment. This microenvironment-responsive hydrogel provides a new therapeutic strategy for precise sequential repair of acute infectious wounds.
{"title":"Microenvironment-feedback hydrogel for precise sequential repair of acute infectious wounds","authors":"Zixuan Tang , Qingquan Xia , Jian Li , Jun Chen , Xuhua Wu , Jiang Li , Jiangyi Liu , Wei Liu , Ke Rong , Xiangchao Meng","doi":"10.1016/j.bmt.2025.100120","DOIUrl":"10.1016/j.bmt.2025.100120","url":null,"abstract":"<div><div>The healing of acute infected wounds is a multi-stage and sequential biological process. Traditional antibacterial dressings are usually a simple superposition of antibacterial properties and active ingredients, lacking effective coupling with the wound microenvironment, and it is difficult to accurately match the continuous process of infected wound healing. In this study, a pH-responsive hydrogel of sodium alginate and carboxymethyl chitosan interpenetrating network was constructed, and tannic acid (TA) and zinc-doped bioglass (BAG) were loaded through hydrogen bonding and hydrophobic interactions. In the acidic environment of infection, the enhancement of intermolecular non-covalent interaction leads to the contraction of hydrogel network and the rapid release of TA. In the alkaline environment of healing, the weakening of intermolecular interaction leads to the expansion of hydrogel network and the continuous release of Zn<sup>2+</sup> and Ca<sup>2+</sup>. <em>In vitro</em> biological evaluation showed that the hydrogel had an effective antibacterial effects against <em>E.coli</em> and <em>S.aureus</em>, and effectively regulated immune response. In addition, the hydrogel effectively removed excessive ROS and significantly increase the activity of cellular antioxidant enzymes, thereby accelerating the wound healing process in animal experiment. This microenvironment-responsive hydrogel provides a new therapeutic strategy for precise sequential repair of acute infectious wounds.</div></div>","PeriodicalId":100180,"journal":{"name":"Biomedical Technology","volume":"12 ","pages":"Article 100120"},"PeriodicalIF":0.0,"publicationDate":"2025-11-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145578953","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 : 2025-11-14DOI: 10.1016/j.bmt.2025.100118
Wei Xu , Liwen Song , Qifeng Yu , Shichao Tong , Yi Wang , Yifan Li , Jin Qiu , Zhikun Li
Chemotherapy-induced bone loss in patients with osteosarcoma (OS) has attracted increasing attention worldwide. Previous studies have revealed the interactions between OS cells and osteoclasts via secretion of various cytokines. However, the specific impacts of chemically injured OS cells on osteoclast functions remain unknown. Untargeted metabolomics is a high-throughput analytical technique used to screen potential biomarkers and identify unknown metabolites in various biological samples. In this study, cisplatin (CDDP)-injured OS cell supernatant promoted the osteoclast differentiation of bone marrow macrophages (BMMs). Untargeted metabolomic analysis revealed the metabolic profile of injured OS cells, and FAPy-adenine (FA), which was upregulated by approximately 2000-fold, was identified in the supernatant. FA promoted the osteoclast differentiation of BMMs in a dose-dependent manner. RNA sequencing revealed increased Fc gamma receptor 1 (Fcgr1) expression levels in FA-treated BMMs. Fcgr1 overexpression promoted the osteoclast differentiation of BMMs and Cathepsin K expression, whereas its knockdown inhibited the pro-osteoclast differentiation effect of FA. Furthermore, FA accelerated osteoporosis progression in ovariectomy model rats. Upregulation of Fcgr1 levels promoted bone loss, whereas its silencing inhibited the bone loss induced by FA in ovariectomy model rats. Collectively, these findings suggest that FA released from CDDP-injured OS cells contributes to osteoporosis progression by upregulating Fcgr1 levels, providing new insights into chemotherapy-induced bone loss in patients with OS.
{"title":"Targeting Fcgr1 to repress FAPy-adenine-induced osteoporosis in osteosarcoma receiving chemotherapy","authors":"Wei Xu , Liwen Song , Qifeng Yu , Shichao Tong , Yi Wang , Yifan Li , Jin Qiu , Zhikun Li","doi":"10.1016/j.bmt.2025.100118","DOIUrl":"10.1016/j.bmt.2025.100118","url":null,"abstract":"<div><div>Chemotherapy-induced bone loss in patients with osteosarcoma (OS) has attracted increasing attention worldwide. Previous studies have revealed the interactions between OS cells and osteoclasts via secretion of various cytokines. However, the specific impacts of chemically injured OS cells on osteoclast functions remain unknown. Untargeted metabolomics is a high-throughput analytical technique used to screen potential biomarkers and identify unknown metabolites in various biological samples. In this study, cisplatin (CDDP)-injured OS cell supernatant promoted the osteoclast differentiation of bone marrow macrophages (BMMs). Untargeted metabolomic analysis revealed the metabolic profile of injured OS cells, and FAPy-adenine (FA), which was upregulated by approximately 2000-fold, was identified in the supernatant. FA promoted the osteoclast differentiation of BMMs in a dose-dependent manner. RNA sequencing revealed increased Fc gamma receptor 1 (Fcgr1) expression levels in FA-treated BMMs. Fcgr1 overexpression promoted the osteoclast differentiation of BMMs and Cathepsin K expression, whereas its knockdown inhibited the pro-osteoclast differentiation effect of FA. Furthermore, FA accelerated osteoporosis progression in ovariectomy model rats. Upregulation of Fcgr1 levels promoted bone loss, whereas its silencing inhibited the bone loss induced by FA in ovariectomy model rats. Collectively, these findings suggest that FA released from CDDP-injured OS cells contributes to osteoporosis progression by upregulating Fcgr1 levels, providing new insights into chemotherapy-induced bone loss in patients with OS.</div></div>","PeriodicalId":100180,"journal":{"name":"Biomedical Technology","volume":"12 ","pages":"Article 100118"},"PeriodicalIF":0.0,"publicationDate":"2025-11-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145528855","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 : 2025-11-14DOI: 10.1016/j.bmt.2025.100119
Xuechao Liu , Kunpeng Wei , Enyu Lin , Yi Li , Pengzhen Zhuang , Yanbing Zhou , Guilai Zuo , Zhaojian Niu
Cancer drug resistance presents a significant challenge in modern oncology, necessitating detailed exploration of its underlying mechanisms and the development of effective counterstrategies. This review aims to systematically evaluate the most recent applications and advancements of multi-omics technologies in elucidating the mechanisms of cancer drug resistance. Multi-omics includes genomics, transcriptomics, proteomics, microbiomics, metabolomics, and epigenomics. Notably, emerging methodologies such as single-cell and spatial omics have been instrumental in revealing the biological characteristics and resistance mechanisms of tumor cells across various layers and dimensions. The review highlights resistance mechanisms uncovered through the combined application of multi-omics, including gene mutations and epigenetic modifications, reprogramming of signaling pathways, drug efflux and cytoskeletal reorganization, and DNA repair mechanisms. It also explores novel mechanisms in the tumor immune microenvironment (TIME), metabolic reprogramming, and microbiome interactions. The review assesses the benefits of integrating multi-omics data, the application of these technologies in identifying key genes and pathways, and their role in personalized treatment strategies. It provides a comprehensive understanding of the dynamic changes and heterogeneity in cancer drug resistance to aid precision treatment strategies. Additionally, the article offers insights into the future directions of multi-omics technologies in oncology drug resistance research and discusses the primary challenges ahead. We aim to provide novel perspectives and directions for innovation and optimization in cancer treatment, ultimately enhancing patient prognosis and quality of life in oncology.
{"title":"Multi-omics advances in understanding cancer drug resistance","authors":"Xuechao Liu , Kunpeng Wei , Enyu Lin , Yi Li , Pengzhen Zhuang , Yanbing Zhou , Guilai Zuo , Zhaojian Niu","doi":"10.1016/j.bmt.2025.100119","DOIUrl":"10.1016/j.bmt.2025.100119","url":null,"abstract":"<div><div>Cancer drug resistance presents a significant challenge in modern oncology, necessitating detailed exploration of its underlying mechanisms and the development of effective counterstrategies. This review aims to systematically evaluate the most recent applications and advancements of multi-omics technologies in elucidating the mechanisms of cancer drug resistance. Multi-omics includes genomics, transcriptomics, proteomics, microbiomics, metabolomics, and epigenomics. Notably, emerging methodologies such as single-cell and spatial omics have been instrumental in revealing the biological characteristics and resistance mechanisms of tumor cells across various layers and dimensions. The review highlights resistance mechanisms uncovered through the combined application of multi-omics, including gene mutations and epigenetic modifications, reprogramming of signaling pathways, drug efflux and cytoskeletal reorganization, and DNA repair mechanisms. It also explores novel mechanisms in the tumor immune microenvironment (TIME), metabolic reprogramming, and microbiome interactions. The review assesses the benefits of integrating multi-omics data, the application of these technologies in identifying key genes and pathways, and their role in personalized treatment strategies. It provides a comprehensive understanding of the dynamic changes and heterogeneity in cancer drug resistance to aid precision treatment strategies. Additionally, the article offers insights into the future directions of multi-omics technologies in oncology drug resistance research and discusses the primary challenges ahead. We aim to provide novel perspectives and directions for innovation and optimization in cancer treatment, ultimately enhancing patient prognosis and quality of life in oncology.</div></div>","PeriodicalId":100180,"journal":{"name":"Biomedical Technology","volume":"12 ","pages":"Article 100119"},"PeriodicalIF":0.0,"publicationDate":"2025-11-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145528256","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 : 2025-11-06DOI: 10.1016/j.bmt.2025.100117
Junxian Cao , Xiao Chang , Shiwen Deng , Hongjun Yang , Gang Guo , Peng Chen
Tuberous sclerosis complex mutation renal angiomyolipomas (TSC-RAML) are benign tumors driven by abnormal growth of mesenchymal-derived cells. Although mTOR inhibitors are clinically used, drug resistance and incomplete tumour shrinkage highlight the need for new treatment approaches. Here, we developed a new strategy combining single-cell transcriptomics, network pharmacology, and functional experiments to identify targeted therapies for TSC-RAMLs. Single-cell RNA sequencing of tumour tissues from 4 TSC-RAML patients uncovered a distinct mesenchymal subpopulation (TSC-RAML-Cells) with upregulated pathways in adipogenesis and mTOR signalling. Using high-dimensional weighted gene co-expression network analysis (hdWGCNA) on TSC-RAML-Cells, we identified three disease-associated modules containing hub genes critical for tumour survival. Cross-referencing these modules with the Connectivity Map (CMAP) drug database prioritized AS-605240 as a potential therapeutic candidate. Protein-protein interaction (PPI) network analysis further revealed PI3KCA as a central target, and molecular dynamics simulations confirmed stable binding between AS-605240 and PI3KCA, with a binding free energy of −7.8 kcal/mol, supporting its mechanism of action. In vitro experiments using patient-derived TSC-RAML cells showed that AS-605240 suppressed cell growth in a dose-dependent manner (IC50 = 7.8 μM) and increased apoptosis rates through inhibition of the PI3K/AKT pathway. This work not only proposes AS-605240 as a promising therapy for TSC-RAMLs but also provides a scalable “cell subtype-to-drug" discovery framework. By integrating single-cell omics and computational drug repurposing, this approach accelerates precision medicine development for rare diseases.
{"title":"Integrative cell subtype-to-drug discovery technology for angiomyolipomas treatment","authors":"Junxian Cao , Xiao Chang , Shiwen Deng , Hongjun Yang , Gang Guo , Peng Chen","doi":"10.1016/j.bmt.2025.100117","DOIUrl":"10.1016/j.bmt.2025.100117","url":null,"abstract":"<div><div>Tuberous sclerosis complex mutation renal angiomyolipomas (TSC-RAML) are benign tumors driven by abnormal growth of mesenchymal-derived cells. Although mTOR inhibitors are clinically used, drug resistance and incomplete tumour shrinkage highlight the need for new treatment approaches. Here, we developed a new strategy combining single-cell transcriptomics, network pharmacology, and functional experiments to identify targeted therapies for TSC-RAMLs. Single-cell RNA sequencing of tumour tissues from 4 TSC-RAML patients uncovered a distinct mesenchymal subpopulation (TSC-RAML-Cells) with upregulated pathways in adipogenesis and mTOR signalling. Using high-dimensional weighted gene co-expression network analysis (hdWGCNA) on TSC-RAML-Cells, we identified three disease-associated modules containing hub genes critical for tumour survival. Cross-referencing these modules with the Connectivity Map (CMAP) drug database prioritized AS-605240 as a potential therapeutic candidate. Protein-protein interaction (PPI) network analysis further revealed PI3KCA as a central target, and molecular dynamics simulations confirmed stable binding between AS-605240 and PI3KCA, with a binding free energy of −7.8 kcal/mol, supporting its mechanism of action. In vitro experiments using patient-derived TSC-RAML cells showed that AS-605240 suppressed cell growth in a dose-dependent manner (IC50 = 7.8 μM) and increased apoptosis rates through inhibition of the PI3K/AKT pathway. This work not only proposes AS-605240 as a promising therapy for TSC-RAMLs but also provides a scalable “cell subtype-to-drug\" discovery framework. By integrating single-cell omics and computational drug repurposing, this approach accelerates precision medicine development for rare diseases.</div></div>","PeriodicalId":100180,"journal":{"name":"Biomedical Technology","volume":"12 ","pages":"Article 100117"},"PeriodicalIF":0.0,"publicationDate":"2025-11-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145473559","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}
Chronic infection with the hepatitis B virus (HBV) is a common cause of liver disease worldwide, particularly in Asia and Africa, where it is highly prevalent. Currently, therapies for chronic HBV infection, such as nucleoside analogs (NAs), mainly suppress viral replication but rarely achieve a lasting cure. Recently, emerging adoptive cell therapy (ACT), represented by chimeric antigen receptor (CAR)-T, T cell receptor (TCR)-T, and CAR-NK (Natural Killer) cell therapy, have provided new opportunities for the treatment of numerous diseases. For instance, CAR-T cells can be designed to target HBV antigens and kill HBV-infected cells with safety concerns regarding potential side effects and limitations of CAR-T cell exhaustion. TCR-T cells mainly exert their immune activation effects by recognizing antigen peptide-MHC complexes in HBV-infected hepatocytes. Although the antiviral effects of TCR-T are evident in preclinical studies, they are limited by on-target toxicity and carry a risk of transient liver damage. In addition to CAR-T and TCR-T therapies, CAR-NK cell therapy has shown promising prospects in treating HBV-associated liver diseases. To enhance the safety and efficiency of ACT applications in clinical settings, CAR and TCR structures should be rationally optimized, and combined treatment strategies need to be explored. In this review, we summarize the structure and mechanism of ACT, including CAR-T, TCR-T, and CAR-NK cell therapies, as well as their research progress and challenges in the treatment of HBV-associated liver diseases.
{"title":"Adoptive cell therapy for HBV-associated liver diseases","authors":"Youxi Zhou , Kaizhao Chen , Yang Zhang , Hongwei Cheng , Shuaishuai Zhang","doi":"10.1016/j.bmt.2025.100116","DOIUrl":"10.1016/j.bmt.2025.100116","url":null,"abstract":"<div><div>Chronic infection with the hepatitis B virus (HBV) is a common cause of liver disease worldwide, particularly in Asia and Africa, where it is highly prevalent. Currently, therapies for chronic HBV infection, such as nucleoside analogs (NAs), mainly suppress viral replication but rarely achieve a lasting cure. Recently, emerging adoptive cell therapy (ACT), represented by chimeric antigen receptor (CAR)-T, T cell receptor (TCR)-T, and CAR-NK (Natural Killer) cell therapy, have provided new opportunities for the treatment of numerous diseases. For instance, CAR-T cells can be designed to target HBV antigens and kill HBV-infected cells with safety concerns regarding potential side effects and limitations of CAR-T cell exhaustion. TCR-T cells mainly exert their immune activation effects by recognizing antigen peptide-MHC complexes in HBV-infected hepatocytes. Although the antiviral effects of TCR-T are evident in preclinical studies, they are limited by on-target toxicity and carry a risk of transient liver damage. In addition to CAR-T and TCR-T therapies, CAR-NK cell therapy has shown promising prospects in treating HBV-associated liver diseases. To enhance the safety and efficiency of ACT applications in clinical settings, CAR and TCR structures should be rationally optimized, and combined treatment strategies need to be explored. In this review, we summarize the structure and mechanism of ACT, including CAR-T, TCR-T, and CAR-NK cell therapies, as well as their research progress and challenges in the treatment of HBV-associated liver diseases.</div></div>","PeriodicalId":100180,"journal":{"name":"Biomedical Technology","volume":"12 ","pages":"Article 100116"},"PeriodicalIF":0.0,"publicationDate":"2025-11-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145473558","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}
扫码关注我们
求助内容：
应助结果提醒方式：
京公网安备 11010802042870号