Biomaterials最新文献

{"title":"Regulating HIF-2α stabilization with an intelligent switchable nanoplatform for tumor immunity reprogramming and enhanced therapy","authors":"Zelun Li ,&nbsp;Guanhua Qiu ,&nbsp;Wenwen Guo ,&nbsp;Yuanquan Zhao ,&nbsp;Yangchun Du ,&nbsp;Huimin Li ,&nbsp;Fumao Yang ,&nbsp;Guozhen Huang ,&nbsp;Ruibiao Fu ,&nbsp;Yan Zou ,&nbsp;Tingting Tan ,&nbsp;Jie Chen ,&nbsp;Xiaofeng Dong","doi":"10.1016/j.biomaterials.2026.124022","DOIUrl":"10.1016/j.biomaterials.2026.124022","url":null,"abstract":"<div><div>Chronic hypoxia is a critical barrier to the effective treatment of solid tumors, including hepatocellular carcinoma (HCC), as it not only restricts the oxygen supply required for sonodynamic therapy (SDT) but also upregulates hypoxia-inducible factor-2α (HIF-2α), thereby accelerating tumor progression, inducing abnormal angiogenesis, suppressing antitumor immune responses, and diminishing the efficacy of targeted therapies. Here, we developed an intelligent switchable organic–inorganic hybrid nanoplatform (VitK3/P–Ce6@H–MnO₂) that integrates oxygen self-supply, reactive oxygen species (ROS) storm induction, and immune microenvironment reprogramming. The acidic tumor microenvironment serves as an “endogenous switch,” triggering the decomposition of H–MnO₂ to release oxygen and Vitamin K3, thereby alleviating chronic hypoxia, facilitating HIF-2α degradation, and providing oxygen support for Ce6-mediated SDT. Upon ultrasound exposure as an “exogenous switch,” activated Ce6, together with Vitamin K3 and Mn²⁺, induces a robust ROS storm, resulting in mitochondrial dysfunction and immunogenic cell death (ICD), while effectively reprogramming the chronic hypoxia–HIF-2α-driven immunosuppressive tumor microenvironment. Furthermore, in vivo studies demonstrated that Lenvatinib therapy, when combined with the nanoplatform, further suppressed chronic hypoxia–HIF-2α–driven abnormal angiogenesis, enhanced CD8⁺ T-cell infiltration, and boosted antitumor immune responses, ultimately achieving a potent synergistic therapeutic effect and promoting the conversion of “cold tumors” into “hot tumors.” This study provides strong experimental evidence that nanoplatform-mediated immune microenvironment reprogramming represents a precisely controllable and highly effective therapeutic strategy for solid tumors, with promising translational potential in hepatocellular carcinoma.</div></div>","PeriodicalId":254,"journal":{"name":"Biomaterials","volume":"330 ","pages":"Article 124022"},"PeriodicalIF":12.9,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146075196","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Spatiotemporal 4D-printed shape-memory scaffold with a triple-acting liposomal strategy for the treatment of infectious bone defects","authors":"Xulin Hu ,&nbsp;Shuhao Yang ,&nbsp;Qianshui Hu ,&nbsp;Zhengguang Pu ,&nbsp;Yingkun Hu ,&nbsp;Wang Gong ,&nbsp;Haoming Wu ,&nbsp;Zhixiang Gao ,&nbsp;Jun Wang ,&nbsp;Jianye Yang ,&nbsp;Yao Zhang ,&nbsp;Xin Yong ,&nbsp;Leilei Qin ,&nbsp;Ning Hu","doi":"10.1016/j.biomaterials.2026.124020","DOIUrl":"10.1016/j.biomaterials.2026.124020","url":null,"abstract":"<div><div>Infectious bone defects (IBD) are complex bone tissue injuries caused by pathogenic bacterial invasion, characterized by delayed bone healing due to bacterial infection and chronic inflammation. In this study, we developed an adaptive filling shape memory scaffold (PTC@PS-EGCG) with temporal and spatial sequence regulation capabilities, integrating multiple functions including antibacterial, immune modulation, and osteogenic induction. The shape memory scaffold (PT) was fabricated using low-temperature 4D printing technology, and a pH-responsive chitosan hydrogel (CS) was used to load phosphatidylserine-modified epigallocatechin gallate liposomes (PS-EGCG) on the scaffold surface to form a coating. The PTC@PS-EGCG scaffold can achieve adaptive filling and integration of irregular defect interfaces at body temperature (37 °C) while providing mechanical support. In the early stages of infection, PS-EGCG is released in response to the infection, clearing bacteria and being phagocytosed by macrophages. Subsequently, PS-EGCG promotes metabolic reprogramming by regulating macrophage oxidative phosphorylation, achieving a “triple effect.” In the middle and late stages, the internal scaffold continues to sustain bone formation. In a rat model of IBD, the PTC@PS-EGCG significantly reduced the expression of inflammatory cytokines and bacterial load, promoted bone regeneration, and improved gait function. This integrated scaffold provides a promising and reliable solution for the clinical treatment of IBD.</div></div>","PeriodicalId":254,"journal":{"name":"Biomaterials","volume":"330 ","pages":"Article 124020"},"PeriodicalIF":12.9,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146075207","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Biosponge-armored polydopamine-modified conducting polypyrrole restores redox-iron homeostasis for enhanced neuroprotection​ in retinal ischemia-reperfusion injury","authors":"Zhiqing Lin ,&nbsp;Haoyue Deng ,&nbsp;Guang Yang ,&nbsp;Keke Huang","doi":"10.1016/j.biomaterials.2026.124007","DOIUrl":"10.1016/j.biomaterials.2026.124007","url":null,"abstract":"<div><div>Retinal ischemia-reperfusion injury (RIRI) is a central pathological mechanism in vision-impairing disorders such as glaucoma and retinal vascular occlusion. Current treatment modalities are significantly constrained by their inability to simultaneously address the multifaceted injury cascades driven by lethal oxidative stress, ferroptosis, and neuroinflammation, which considerably limits their clinical efficacy. To overcome these challenges, we designed a nanocomposite, termed P-PPy, by integrating polydopamine with conducting polypyrrole. Within this construct, surface-modified polydopamine (PDA) acts as a biosponge that effectively chelates excess iron ions. A single intravitreal injection of P-PPy elicited broad therapeutic responses, including efficient reactive oxygen species (ROS) scavenging, inhibition of ferroptosis in retinal ganglion cells accompanied by restoration of mitochondrial functionality, and induction of M2 microglial polarization leading to attenuated neuroinflammation. Together, these mechanisms synergistically restored the electrophysiological microenvironment of the retina, markedly preserving both its structural integrity and functional performance. The P-PPy nanocomposite also demonstrated an excellent biosafety profile, exhibiting no detectable toxicity in both cellular assays and following intravitreal administration in animal models. In summary, this readily synthesizable, multifunctional conductive nanoplatform provides strong neuroprotective effects in vivo, offering a promising therapeutic avenue based on conductive nanomaterials for the treatment of neurodegenerative retinal diseases.</div></div>","PeriodicalId":254,"journal":{"name":"Biomaterials","volume":"330 ","pages":"Article 124007"},"PeriodicalIF":12.9,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146024836","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Spatiotemporally programmed VEGF/IL-4 delivery via HMSNs enhances endothelialization and immune-mediated matrix remodeling in acellular vascular grafts","authors":"Zeguo Chen ,&nbsp;Zhongshi Wu ,&nbsp;Can Huang ,&nbsp;Qiying Wu ,&nbsp;Chao Xie ,&nbsp;Sicheng Chen ,&nbsp;Liang Yi ,&nbsp;Haoyong Yuan ,&nbsp;Sixi Liu ,&nbsp;Abdulraheem Mustapha ,&nbsp;Siyao Chen ,&nbsp;Wansong Chen ,&nbsp;Ting Lu ,&nbsp;Zhenjie Tang ,&nbsp;Yuhong Liu","doi":"10.1016/j.biomaterials.2026.124016","DOIUrl":"10.1016/j.biomaterials.2026.124016","url":null,"abstract":"<div><div>Delayed endothelialization and inadequate matrix remodeling remain major obstacles in the development of small-diameter vascular grafts (SDVGs; &lt;6 mm). To address these challenges, we developed an immunomodulatory tissue-engineered vascular graft (iTEVG) by integrating hollow mesoporous silica nanoparticles (HMSNs) with tailored mesopore sizes as delivery carriers for immunoregulatory factors. VEGF was selectively immobilized on the intimal surface, while the adventitia incorporated a sequential release system for VEGF and IL-4. VEGF exhibited rapid release (64.04 ± 4.44 % in 7 days), promoting monocyte recruitment and adventitial neovascularization, while IL-4 showed sustained release (65.94 ± 2.06 % over 28 days), driving long-term M2 macrophage polarization. In rats, iTEVGs achieved 88 % endothelial coverage and smooth muscle cell infiltration within 1 month, full-thickness cellularization with a complete trilaminar structure by 3 months, and maintained mechanical integrity without aneurysm formation up to 6 months. This spatially partitioned platform, built on an acellular vascular scaffold, enables precise spatiotemporal regulation of the immune microenvironment and offers a design paradigm that synergistically promotes endothelialization and vascular matrix remodeling. The “intima-targeted regeneration and adventitia-sequential-release” strategy provides a promising template for SDVG design that may be extended to other complex organ constructs.</div></div>","PeriodicalId":254,"journal":{"name":"Biomaterials","volume":"330 ","pages":"Article 124016"},"PeriodicalIF":12.9,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146074807","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Spatiotemporal controls of neutrophil extracellular traps boosts neutrophils immunotherapy efficiency against solid tumors","authors":"Lingxiao Jin ,&nbsp;Liang Chen ,&nbsp;Yucheng Xue ,&nbsp;Keye Chen ,&nbsp;Shixin Chen ,&nbsp;Kelei Wang ,&nbsp;Fangqian Wang ,&nbsp;Guoxin Qu ,&nbsp;Zhenxuan Shao ,&nbsp;Shenzhi Zhao ,&nbsp;Haochen Mou ,&nbsp;Hao Zhou ,&nbsp;Zengjie Zhang ,&nbsp;Xiayu Hu ,&nbsp;Jiangchu Lei ,&nbsp;Fanglu Chen ,&nbsp;JianBin Xu ,&nbsp;Peng Zhang ,&nbsp;Binghao Li","doi":"10.1016/j.biomaterials.2026.124012","DOIUrl":"10.1016/j.biomaterials.2026.124012","url":null,"abstract":"<div><div>Neutrophils have emerged as promising candidates for next-generation immunotherapies against solid tumors. However, the physical barrier formed by tumor-induced neutrophil extracellular traps (NETs) significantly restricts the migration and infiltration of circulating immune cells, thereby limiting their anti-tumor efficacy. This study demonstrated tumors driven NET formation.</div><div>within recruited neutrophils via the Transforming Growth Factor Beta (TGFβ) signaling pathway. Therefore, a neutrophil-arming nanoplatform (NE@LTT@DNase1) was developed to enable neutrophils to degrade NETs while preserving their innate immune functions. Mechanistically, NE@LTT@DNase1 exerts dual therapeutic effects: (i) enzymatic degradation of pre-existing NETs via neutrophil surface-anchored DNase1 and (ii) spatiotemporal suppression of NETosis via endogenous lysine-trypotophan-threonine peptide (LTT) fragmentation in a reactive oxygen species-dependent manner. Data show that NE@LTT@DNase1 treatment was associated with increased infiltration of NK cells and T cells, as well as a shift of neutrophils and macrophages toward an anti-tumor polarization, collectively contributing to the reversal of the immunosuppressive tumor microenvironment (TME). In combination with anti-Programmed Death-1 (anti-PD-1) therapy, the NE@LTT@DNase1-based immunotherapy strategy resulted in a 74 % reduction in tumor burden and prolonged median survival by 61 % in tumor-bearing mice. Overall, these findings established a next-generation therapeutic paradigm for advanced neutrophil-based immunotherapy (NBI).</div></div>","PeriodicalId":254,"journal":{"name":"Biomaterials","volume":"330 ","pages":"Article 124012"},"PeriodicalIF":12.9,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146049783","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Ultrasound-activated metal-polyphenol nanodroplets for tumor cuproptosis","authors":"Ning Cong ,&nbsp;Lu Guo ,&nbsp;Xiaoxuan Wang ,&nbsp;Yading Zhao ,&nbsp;Ting Zhao ,&nbsp;Shuting Huang ,&nbsp;Rui Liu ,&nbsp;Song Ning ,&nbsp;Xiaoying Zhou ,&nbsp;Suyun Li ,&nbsp;Yuye Fu ,&nbsp;Jie Li","doi":"10.1016/j.biomaterials.2026.124013","DOIUrl":"10.1016/j.biomaterials.2026.124013","url":null,"abstract":"<div><div>Cuproptosis is a novel form of cell death that relies on mitochondrial metabolism and has opened up new avenues for tumor therapy. However, resistance to cuproptosis in tumors can arise from several factors, such as their reliance on aerobic glycolysis, the high-glutathione (GSH) environment, and inefficient copper (Cu) delivery. In this study, we developed shell-core nanodroplets (NDs) approximately 280 nm in diameter, named Cu-EGCG-SHK-NDs. These NDs are composed of a liquid-gas phase-change perfluorohexane core and a carboxymethyl chitosan shell, loaded with the glycolytic inhibitor shikonin (SHK) and coated with Cu-complexed epigallocatechin gallate (Cu-EGCG), enabling targeted delivery through ultrasound (US)-targeted microbubble destruction (UTMD). The dual responsiveness of NDs to both US and pH enables precise drug release and efficient intracellular uptake. In addition, the US response enhances contrast-enhanced US imaging and triggers the generation of reactive oxygen species, subsequently depleting GSH. Both <em>in vitr</em><em>o</em> and <em>in vivo</em> experiments confirm that Cu-EGCG-SHK-NDs possess excellent biocompatibility. Combined with UTMD, they can efficiently co-deliver Cu and SHK into tumour cells, inhibit glycolytic metabolism, and significantly reduce intracellular GSH levels. This synergistic mechanism enhances cuproptosis induction and achieves effective tumour growth inhibition.</div></div>","PeriodicalId":254,"journal":{"name":"Biomaterials","volume":"330 ","pages":"Article 124013"},"PeriodicalIF":12.9,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146024834","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Inhalable DNA nano-adjuvant elicits robust lung-resident memory immunity against pneumonic plague","authors":"Shengnan Fu ,&nbsp;Zhixin Li ,&nbsp;Zhe Yin ,&nbsp;Xi Zhang ,&nbsp;Xiaolin Song ,&nbsp;Lingfei Hu ,&nbsp;Dongsheng Zhou ,&nbsp;Xin Su ,&nbsp;Chenxi Dai","doi":"10.1016/j.biomaterials.2026.124009","DOIUrl":"10.1016/j.biomaterials.2026.124009","url":null,"abstract":"<div><div>Pneumonic plague, caused by <em>Yersinia pestis</em>, remains a deadly threat due to its high mortality and rapid progression. In our previous study, <em>Yersinia pestis</em> antigens formulated with CpG oligodeoxynucleotides show great potential against pneumonic plague, but these agonists display low TLR9 affinity, poor stability, limited cellular uptake, and weak induction of tissue-resident memory immunity. Here, we introduce AdjCRU, a cruciform DNA nano-adjuvant built on a four-way junction with each arm presenting looped CpG motifs (LoDNA) for TLR9 engagement. Guided by computational design and molecular dynamics simulations, the four-way junction is chosen over other nanostructures for superior TLR9 binding. AdjCRU is nuclease-resistant, prepared by one-step annealing of four single-stranded oligonucleotides. When administered via aerosolized intratracheal inoculation alongside <em>Yersinia pestis</em> recombinant antigen rV10, AdjCRU is effectively internalized into lysosomes of antigen-presenting cell (APC), inducing markedly enhanced APC maturation, germinal center reaction, systemic and mucosal antibody titers, and T/B cell activation. Notably, rV10+AdjCRU drives robust lung-resident memory T/B cell immunity, and significantly improves survival by 40 % over free LoDNA in a lethal pneumonic plague mouse model. By integrating programmability, biocompatibility, and enhanced TLR9 stimulation into a single, modular platform, AdjCRU offers a versatile strategy for next-generation mucosal adjuvants against respiratory pathogens.</div></div>","PeriodicalId":254,"journal":{"name":"Biomaterials","volume":"330 ","pages":"Article 124009"},"PeriodicalIF":12.9,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146024837","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"FAK modulates immune response and fibroblast activation in biomaterial-induced fibrosis","authors":"Marc A. Fernández-Yagüe ,&nbsp;Graham F. Barber ,&nbsp;Aránzazu del Campo ,&nbsp;Andrés J. García","doi":"10.1016/j.biomaterials.2026.124010","DOIUrl":"10.1016/j.biomaterials.2026.124010","url":null,"abstract":"<div><div>Fibrotic capsule formation remains a major barrier in the clinical performance of biomedical implants. Here, we demonstrate that synthetic hydrogels mimicking the mechanical properties of fibrotic tissue trigger stromal cell activation and immune remodeling via focal adhesion kinase (FAK)-mediated mechanotransduction. Using a mechanically tunable poly(ethylene glycol) hydrogel platform and subcutaneous implantation in mice, we show that pharmacological inhibition of FAK activity significantly reduces α-smooth muscle actin (α-SMA)-positive myofibroblast activation, collagen I deposition, and fibrotic capsule thickness in a hydrogel stiffness-dependent manner. Flow cytometry and cytokine profiling revealed that FAK inhibition alters the fibrotic niche by reducing CD163-positive M2c macrophages and significantly downregulating pro-fibrotic cytokines including IL-6, and VEGF, while transiently increasing regulatory T cells and elevating IL-10 levels. Importantly, these changes occurred without parallel increases in canonical pro-inflammatory cytokines, indicating selective modulation rather than global immune suppression or activation. These findings position FAK as a central hub translating mechanical cues into coordinated stromal and immune responses. Targeting FAK mechanotransduction may provide a therapeutic strategy to mitigate foreign body responses and improve implant integration across regenerative applications.</div></div>","PeriodicalId":254,"journal":{"name":"Biomaterials","volume":"330 ","pages":"Article 124010"},"PeriodicalIF":12.9,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146024838","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Harnessing the HMnO2 nanoparticles as the DNA injury amplifier to improve the OXA-based trans-artery infusion chemotherapy","authors":"Xianting Sun ,&nbsp;Cai Feng ,&nbsp;Zongling Xiong ,&nbsp;Yifei Yang ,&nbsp;Hao Zhou ,&nbsp;Tianming Wang ,&nbsp;Xiaofen Wang ,&nbsp;Shulin Liu ,&nbsp;Sai Li ,&nbsp;Peng Lei ,&nbsp;Liangrong Shi ,&nbsp;Weihua Liao","doi":"10.1016/j.biomaterials.2026.123993","DOIUrl":"10.1016/j.biomaterials.2026.123993","url":null,"abstract":"<div><div>Oxaliplatin (OXA) serves as a key chemotherapeutic agent in trans-arterial infusion chemotherapy (TAIC) for liver cancer. However, its clinical efficacy is frequently limited by several factors: suboptimal tumor uptake, systemic detoxification mediated by glutathione (GSH), and the activation of cellular DNA repair mechanisms. Herein, we present a hollow MnO₂ nanoparticle loaded with OXA, the PEI-HMnO₂@OXA, to improve the TAIC effect of OXA. The acidic tumor microenvironment facilitated the release of OXA and triggered PEI-HMnO₂ to generate free radicals. When coupled with GSH depletion, this cascade culminated in significant DNA damage. Moreover, the PEI-HMnO₂ showed a synergistic effect with OXA by blocking multiple DNA repair genes. On the other hand, by leveraging the enhanced permeability and retention effect of the nano-sized structure, 10–100 times greater tumor uptake and a more pronounced inhibitory effect by TAIC are achieved compared with intravenous or single-drug treatment. Meanwhile, the PEI-HMnO₂@OXA enabled real-time MRI monitoring of drug distribution and tumor state, facilitating the treatment guidance. Comprehensive experiments using different cell lines, mouse and rabbit models, and patient-derived HCC OXA-sensitive/resistant organoids were conducted to clarify the tumor-inhibiting effects of PEI-HMnO₂@OXA, providing novel insights into cancer management.</div></div>","PeriodicalId":254,"journal":{"name":"Biomaterials","volume":"330 ","pages":"Article 123993"},"PeriodicalIF":12.9,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145975836","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Near-infrared orthogonal excitation lanthanide theranostic nanoplatform for NIR-II-L imaging-guided photodynamic therapy via synergistical pyroptosis and apoptosis pathway","authors":"Jialing Zhou ,&nbsp;Jiang Ming ,&nbsp;Zhenfeng Yu ,&nbsp;Zhihua Wang ,&nbsp;Wenlin Li ,&nbsp;Ahmed Mohamed El-Toni ,&nbsp;Aliyah Almomen ,&nbsp;Aibin Liang ,&nbsp;Yong Fan ,&nbsp;Fan Zhang","doi":"10.1016/j.biomaterials.2026.123994","DOIUrl":"10.1016/j.biomaterials.2026.123994","url":null,"abstract":"<div><div>Photodynamic therapy (PDT) that induces pyroptosis at the cell membrane has emerged as a promising paradigm for cancer immunotherapy. However, the rapid and precise induction of pyroptosis remains a significant challenge. To address this, we developed a near-infrared orthogonal excitation lanthanide theranostic nanoplatform based on lanthanide doped nanoparticles conjugated with curcumin (CUR) and cyclo(RGD-DPhe-K) peptide (LnNP@CUR-RGD). This platform enables deep-tissue, NIR-II-L imaging-guided PDT that concurrently initiates both pyroptosis and apoptosis. Upon 808 nm excitation, fluorescence at 1530 nm from LnNP@CUR-RGD allows for real-time in vivo tracking and monitoring of its localization to the cell membrane or lysosome. After subsequently switching to 940 nm excitation, the produced 362 nm emission activates CUR to generate singlet oxygen (¹O₂). This process initiates a dual-death mechanism: cell membrane-involved pyroptosis and lysosome-involved apoptosis, which synergistically potentiate the anti-tumor immune response. Notably, this nanoplatform achieves efficient antitumor therapy within 15 min of systemic administration, a significant acceleration compared to the 6 h required for conventional apoptosis-based PDT. This work demonstrates the considerable potential of NIR-light-triggered, targeted theranostic platforms for precise imaging-guided cancer therapy.</div></div>","PeriodicalId":254,"journal":{"name":"Biomaterials","volume":"330 ","pages":"Article 123994"},"PeriodicalIF":12.9,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146008015","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}