Biomaterials research最新文献

Bone homeostasis is a dynamically orchestrated process that is intricately regulated by the immune system. The emerging field of osteoimmunology has demonstrated that bone homeostasis and repair are governed by a sophisticated crosstalk between immune and skeletal cells, in which immune signals play a critical role in modulating osteogenesis and osteoclastogenesis. Nevertheless, conventional bone repair strategies frequently overlook immune modulation, instead prioritizing structural support or direct osteoinductive effects. Exosomes-endogenous nanovesicles characterized by low immunogenicity and high bioavailability-have emerged as potent mediators within the immune-bone axis. These vesicles mediate intercellular communication by delivering functional cargo, including miRNAs, proteins, and lipids, across biological barriers, thereby enabling precise regulation of inflammatory responses and immune cell polarization. Importantly, exosomes can reprogram the local immune microenvironment from a pro-inflammatory to a regenerative, anti-inflammatory state, thus promoting enhanced bone healing in complex clinical conditions such as osteoporosis and bone defects. This review systematically examines the molecular mechanisms through which exosomes modulate immune responses in bone biology, highlights their pivotal role in reshaping the osteoimmune microenvironment, and discusses their transformative potential in the development of next-generation, precision-based therapeutic approaches for bone regeneration.

The International Union of Societies for Biomaterials Science and Engineering (IUSBSE) is a global organization in the field of biomaterials that brings together national and international biomaterials societies. It is dedicated to the advancement of not only biomaterials but also surgical implants, prosthetics, artificial organs, tissue engineering, drug delivery, and regenerative medicine. IUSBSE and the World Biomaterials Congress were established in 1996. This article highlights the efforts and contributions of IUSBSE's past and current presidents from 1980 to 2024 in both academia and industry. The history of IUSBSE acknowledges its background, its role, and the lifetime contributions of its presidents in fostering international networks among students, researchers, and societies in biomaterials science, as well as advancing academic and industrial progress in support of human health.

Advancements in dental restoration technologies have created transformative opportunities for enhancing crown repair through intelligent sensing and adaptive design. While modern materials like ceramics and resins improve aesthetic and functional outcomes, persistent challenges in long-term fit, durability, and dynamic pressure monitoring remain unaddressed. This study introduces a groundbreaking approach that synergizes 3-dimensional (3D)-printed colloidal crystal hydrogel crowns with machine learning-integrated resistance strain sensors. The hydrogel's inverse opal structure ensures robust adhesion to the tooth surface, while embedded strain sensors capture real-time, multidirectional pressure data. Unlike conventional sensing systems, our framework employs machine learning algorithms to dynamically interpret strain patterns, enabling predictive modeling of occlusal forces and adaptive calibration of crown fit. The hydrogel's temperature-responsive properties, combined with sensor stability under oral environmental fluctuations, ensure reliable long-term performance. Machine learning further enhances diagnostic precision by correlating strain-resistance data with clinical parameters, facilitating personalized adjustments to restoration plans. This work pioneers the fusion of intelligent sensing, material innovation, and data-driven analytics in dental care, establishing a foundation for next-generation adaptive and patient-specific restorative solutions.

Conventional treatments for ulcerative colitis (UC) are often associated with systemic side effects and require frequent dosing due to nonspecific drug distribution. Herein, a hydrogel based on poly(diallyldimethylammonium chloride) (PDADMAC) and cellulose nanocrystals (CNCs) was designed for the oral delivery of celecoxib in the treatment of UC. The hydrogel network incorporated sulfate ester groups, enabling sulfatase enzymes sensitive in the colon. Physiochemical characterization confirmed successful formation of the hydrogel, effective sulfate functionalization, and efficient drug encapsulation. Swelling studies revealed that the hydrogel maintained structural stability under different pH conditions, while in vitro and in vivo experiments demonstrated that drug release was markedly enhanced in the presence of sulfatase. Furthermore, the hydrogel showed improved drug loading efficiency and sustained release behavior. In a dextran sulfate sodium-induced UC mouse model, the celecoxib-loaded PDADMAC-CNC hydrogel effectively alleviated colonic inflammation, preserved colon structure, and reduced pro-inflammatory cytokine levels more markedly than free drug administration. This finding highlights the potential of sulfatase-responsive PDADMAC-CNC hydrogels as a targeted, safe, and effective approach for treating inflammatory bowel diseases, such as UC.

Triple-negative breast cancer (TNBC) remains therapeutically challenging owing to the paucity of broadly effective molecular targets. Piezoelectric nanomaterials that generate localized electric fields and reactive oxygen species under ultrasound (US) stimulation have emerged as a promising strategy for TNBC therapy. Here, we developed a US-activatable nanoplatform (HN-T/BT@Lip) in which toyocamycin-loaded CaCO₃-carboxymethyl chitosan hybrid nanoparticles (HNs) and barium titanate (BaTiO₃, BT) are co-encapsulated in folate-modified liposomes. US-activated HN-T/BT@Lip suppressed tumor growth and induced ferroptosis. Integrated transcriptomic, metabolomic, and microbiota profiling further revealed that this treatment disrupts glutathione metabolism, enhances susceptibility to lipid peroxidation, and perturbs iron homeostasis. These effects were closely associated with shifts in microbial community composition and altered levels of microbiota-derived metabolites. In vitro assays further demonstrated that the microbiota-associated metabolite trimethylamine N-oxide synergistically amplified lipid peroxidation under HN-T/BT@Lip + US treatment. Collectively, our findings demonstrate that US-activated HN-T/BT@Lip elicits potent ferroptosis in TNBC while concomitantly reshaping the intratumoral microbiota-metabolism landscape, and they highlight microbiota-derived metabolites such as trimethylamine N-oxide as potential modulators and biomarkers of nanotherapeutic ferroptosis.

Bone-related disorders, including fractures and osteoporosis, remain substantial clinical challenges, partly because of the limited availability of reliable osteogenic cell sources and complications associated with current therapies. To address these limitations, this study introduces a novel protein-based direct reprogramming platform for the conversion of human dermal fibroblasts into functional osteoblasts using only 2 transcription factors, octamer-binding transcription factor 4 (Oct4) and core-binding factor β (Cbfβ), fused to the silkworm-derived cell-penetrating protein, 30Kc19. Genetic fusion with 30Kc19 markedly improves the stability and cellular uptake of both Oct4 and Cbfβ, resulting in recombinant constructs (Oct4-30Kc19 and Cbfβ-30Kc19) that achieve high reprogramming efficiency with negligible cytotoxicity, outperforming plasmid DNA-based methods. The protein-induced osteoblasts (piOBs) exhibit a characteristic osteoblast morphology, express established osteogenic markers, and display a global transcriptomic profile that aligns with key features of primary human osteoblasts. Importantly, transplantation of piOBs into a murine calvarial defect model induces substantial new bone formation, demonstrating in vivo therapeutic efficacy. By leveraging the unique cell-permeable and protein-stabilizing properties of 30Kc19, this streamlined 2-factor system represents a potentially safer, more scalable, and clinically feasible strategy for regenerative therapies targeting bone diseases, circumventing the inherent risks associated with viral vectors and genomic integration.

Background: Metabolic-associated steatotic liver disease (MASLD), including metabolic dysfunction-associated steatohepatitis (MASH), is a growing health concern characterized by liver inflammation, fibrosis, and endothelial dysfunction. Targeted therapies are essential to address these issues and improve treatment outcomes. Methods: A sialic acid (SA)-modified nanomicelle system (SA-PEG-ALA) was developed to target liver sinusoidal endothelial cells (LSECs) via the E-selectin (SELE). Molecular docking and surface plasmon resonance (SPR) were used to confirm the binding interaction between SA and SELE. In vitro assays using LSECs and steatotic hepatocytes were conducted to evaluate the cellular uptake and therapeutic efficacy of SA-PEG-ALA. In vivo studies using an HFHC-induced MASH mouse model were carried out to evaluate the distribution and therapeutic outcomes of SA-PEG-ALA. Additionally, RNA sequencing was performed to explore the molecular mechanisms underlying its effects. Results: Molecular docking and SPR analyses confirmed that SA effectively binds to SELE, facilitating the targeted delivery of ALA to LSECs. In vitro, SA-PEG-ALA showed substantially higher uptake in LSECs compared to other formulations. In vivo, SA-PEG-ALA demonstrated superior targeting of the liver and showed enhanced therapeutic effects compared to PEG-ALA, significantly alleviating steatosis, liver inflammation, and fibrosis in the MASH model. Mechanistically, SA-PEG-ALA interacted with HSP70, enhancing its stability and promoting the binding of HSP70 to IκBα, which contributed to inhibition of NF-κB signaling pathway. Conclusion: SA-PEG-ALA offers a promising targeted therapeutic strategy for MASLD, with improved liver targeting, anti-inflammatory, and antifibrotic effects, highlighting its potential for treating MASLD.

Cancer patients exposed to chemotherapeutic drugs and whole-body radiation can result in testicular injury and germ cell loss. One of the mechanisms is that these drugs lead to the accumulation of reactive oxygen species (ROS) in the testes, which has been documented to cause testicular damage. Therefore, this highlights the critical need for ROS clearance in testes to preserve male fertility during cancer treatment. The blood-testis barrier (BTB) poses a major challenge, due to the absence of effective pharmaceutical agents that can penetrate this barrier to neutralize ROS effectively. We synthesized nanomaterials based on manganese-superoxide dismutase (PCN-222-Mn), demonstrating the ability to cross BTB and facilitate ROS clearance. Real-time T1-weighted magnetic resonance imaging confirmed the targeted delivery of PCN-222-Mn to the testes in mice. In murine models of testicular injury induced by cyclophosphamide, PCN-222-Mn showed major therapeutic effects by protecting germ cells and associated somatic cells through ROS reduction and autophagy enhancement. Additionally, PCN-222-Mn was demonstrated to penetrate Sertoli cells via clathrin-mediated and caveolae-mediated endocytosis and expelled by exocytosis, facilitating transport across the BTB. This research not only proposes a viable therapeutic approach to preserve male fertility during cancer treatment but also underscores the transformative potential of nanozymes in clinical settings.

Tendinopathy is a musculoskeletal disorder characterized by severe pain that may persist for weeks or months, often resulting in disability. Existing treatments primarily consist of conservative interventions, including rest, nonsteroidal anti-inflammatory medications, localized corticosteroid injections, ultrasound, bracing, and stem cell-based therapies, as well as surgical procedures. However, therapeutic outcomes remain unsatisfactory. Consequently, there is an urgent need for effective strategies in tendinopathy management. As a bioengineered material, the hydrogel has been extensively studied for the treatment of tendinopathy due to its stable physicochemical properties, biocompatibility, degradability, mechanical robustness, injectability, and stimuli-responsive drug delivery capability. Based on the anatomical structure of tendons and therapeutic requirements during disease progression, hydrogels can be designed into various formulations, such as scaffolds, patches, sprays, microspheres, and injectable systems, depending on the raw materials, crosslinking methods, sizes, and morphological configuration. This review provides a comprehensive overview of the pathophysiological process involved in tendon healing and summarizes the considerations in the design of hydrogels in tendinopathy treatment. It emphasizes the therapeutic applications and stimuli-responsive properties of various hydrogel formulations in tendinopathy treatment, advancing the understanding of hydrogel-based strategies for tendinopathy management and focusing on formulation design. Additionally, the opportunities artificial intelligence brings to hydrogel research in design, optimization, and application advancement are also comprehensively discussed. Understanding the advances associated with hydrogel development is crucial for tendinopathy treatment.

Diarrheal infections caused by antibiotic-resistant Escherichia coli pose a serious threat to human and animal health, driving the need for innovative therapeutic strategies. This study introduces a dual-action strategy that integrates bacteriophage EC.W2-6 with bentonite to enhance bacterial clearance and macromolecular toxin removal. Phage EC.W2-6 demonstrated high specificity against enterotoxigenic E. coli (ETEC) H10407, achieving nearly 100% adsorption to host cells within 15 min and a moderate burst size of approximately 80 plaque-forming units per infected cell. Bentonite exhibited substantial dose-dependent binding of ETEC-secreted proteins and outer membrane vesicles (OMVs), with the 30-g treatment showing the highest efficiency. Nanoparticle tracking analysis confirmed a 3.56-fold reduction in OMVs at 5 g bentonite and near-complete removal at 30 g. Physicochemical analysis indicated a stabilizing effect of bentonite, showing that bentonite-phage association partially neutralized the phage surface charge (from -34.2 to -13.4 mV), forming a more stable colloidal complex with an approximately 2-fold decrease in colloidal size. In a murine diarrheal model, single therapy with either EC.W2-6 (multiplicity of infection = 0.1) or 8% bentonite conferred 60% survival, whereas combination treatment provided 100% protection with a synergistic effect. Microbiome analysis revealed that dual therapy restored gut microbial diversity and suppressed Proteobacteria expansion, closely resembling healthy controls. These findings highlight the therapeutic potential of combining bentonite with phage therapy as an integrated macromolecular intervention against ETEC-induced diarrhea and intestinal dysbiosis.