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Materials Today Bio · 2026 · IF 11

From targeted delivery to inflammation suppression: engineering plant exosomes for heart failure therapy post-infarction

Xi Tan,Simin Lu,Wangbei Qin,Xiaoqin Zhu,Xinlu Wang,Kaiwei Ren,Biwei Cheng,Jiahui Li,Dongze He,Ziran Hu,Yuhua Lei,Lixing Wu,Jing Zhang,Jiaxin Hu

Plant-derived exosomes are natural nanovesicles rich in bioactive compounds and show promise for tissue regeneration. However, their clinical use is limited by poor stability and low targeting accuracy. To overcome these issues, we developed an engineered approach to enhance the targeted delivery of plant exosomes, focusing on chronic inflammation—a key driver of heart failure—evaluating their therapeutic potential in myocardial infarction. By optimizing isolation methods and fusing exosomes with synthetic liposomes, we created collagen-targeted hybrid nanovesicles (GEP-NPs). In a mouse model of myocardial infarction, GEP-NPs efficiently accumulated in damaged heart tissue. Compared to non-engineered vesicles, GEP-NPs more effectively reduced fibrosis, suppressed ventricular remodeling, and modulated chronic post-infarction inflammation, thereby preventing progression from acute injury to chronic heart failure. Mechanistic studies showed that GEP-NPs may inhibit the overactive PI3K-AKT-mTOR pathway, which regulates inflammation, cell survival, and metabolism. The bioactive components from plant exosomes likely act effectively within the engineered vesicles to suppress this pathway, reducing persistent inflammation and promoting tissue repair. This work provides a scalable, reproducible method for engineering plant exosomes, improving both delivery precision and stability, and offering a promising strategy for treating chronic cardiac inflammation and preventing heart failure.

CAS / MDL: 100068-60-8
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JOURNAL OF EXPERIMENTAL & CLINICAL CANCER RESEARCH · 2026 · IF 14.3

Nanovaccines with ferroptosis, necroptosis and STING-activation for synergistic immunotherapy

Jia-Rui Du,Mu-Le Tu,Yong-Xu Xia,Yuan-Qiang Lin,Rui Yang,Chang Weng,Yi Liu,Hao Zhang,Hui Wang,Wen-Jie Feng,Deng-Ke Teng

Nanovaccines based on immunogenic cell death (ICD) present a promising strategy in tumor immunotherapy, serving as a bridge connecting tumor cell death to the induction of anti-tumor immunity. However, their efficacy is severely limited by the immunologically silent nature of apoptosis-dependent ICD and the immunosuppressive tumor microenvironment (TME). In this work, we designed a metal‒polyphenol network nanovaccine (SRF@FeShik-cGAMP/HA). Upon reaching the tumor tissue through specific targeting, the nanovaccines disassemble within the tumor cells, releasing the Fenton reaction catalyst ferrous iron (Fe 2+ ), the system Xc- inhibitor sorafenib (SRF), and necroptosis inducer shikonin. Fe 2+ , SRF, and shikonin collectively promote the accumulation of lipid peroxide and amplify ferroptosis by providing an exogenous iron source, inhibiting glutathione biosynthesis, and boosting reactive oxygen species production, respectively. Meanwhile, shikonin induces necroptosis. The combination of ferroptosis and necroptosis overcomes the limitation of tumor immune silencing and triggers a strong ICD. Simultaneously, the immune adjuvant 2'3'-cyclic-GMP-AMP (cGAMP) activates the STING pathway, reversing the immunosuppressive TME and enhancing the anti-tumor immune response mediated by ICD. The synergistic action of ferroptosis, necroptosis, and the STING pathway produces a cascade of antitumor immune responses and establishes long-term immune memory. This nanovaccine demonstrates promising therapeutic effects in primary, orthotopic, and recurrent hepatocellular carcinoma (HCC) models. Collectively, our findings present a cancer immunotherapy strategy that exploits dual ferroptosis and necroptosis induction to trigger ICD, bypassing the limitations of apoptosis-dependent pathways. This strategy coordinates with the STING pathway to achieve potent antitumor immunity, providing a promising paradigm for HCC treatment, and offering a promising and translatable path for clinical development.

✓ 已验证 产品关联 DOI PubMed 高影响因子
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TALANTA · 2026 · IF 6.7

Sequential site engineering of an Fe–N4 oxidase-like nanozyme for colorimetric detection of alkaline phosphatase

Xiao Ma,Junjie Wang,Xin Chen,Jingcheng Li,Jiaqi Xue,Yufan Hou,Shihao Zhao,Jingxiang Zhao,Xiaomi Meng,Huajun Chen,Fang Wang,Fangya Guo,Jian Sun,Dan Zhao

Oxidase-like nanozymes use dissolved O 2 as the terminal electron acceptor and do not require exogenous H 2 O 2 , offering methodological advantages; however, conventional “one-pot carbonization” often causes concurrent carbonization and active-site formation, making the coordination environment difficult to control. Here, a sequential “pre-coordinate-polymerize-pyrolyze” site-engineering route was developed. On carbon black, OPD-Fe 3+ pre-coordination and in situ oxidative polymerization were carried out, followed by thermal treatment and purification, by which Fe–N moieties were immobilized within the shell region of the material to afford highly dispersed Fe–N x moieties predominantly featuring Fe–N 4 -like coordination (Fe–N 4 @CB d ). Multiscale characterization (XRD/XPS/XANES/EXAFS) consistently showed that iron resided predominantly in a first coordination sphere dominated by Fe–N (coordination number CN ≈ 3.7; R ≈ 2.01 Å), with no resolvable Fe–Fe scattering and only minor, non-dominant Fe-containing phases. ROS-trapping and time-dependent EPR measurements further confirmed continuous O 2 activation with the generation of O 2 • - , •OH, and 1 O 2 in the Fe–N 4 @CB d /O 2 system. DFT calculations additionally supported Fe–N 4 -like Fe–N x sites as the most plausible dominant active structures for O 2 activation. Under a unified TMB/O 2 system, steady-state enzyme kinetics exhibited outstanding performance, with V max  = 351 nmol L −1  s −1 and K m  = 0.56 mM, which are competitive among reports using the same substrate/readout. An H 2 O 2 -free colorimetric platform for alkaline phosphatase (ALP) was constructed on this material, achieving a low limit of detection and good linearity; acceptable accuracy and precision were verified by standard additions in diluted serum. This sequential strategy predefines the Fe–N neighborhood and topology at the precursor stage, reduces uncertainty in site formation, and avoids metal-organic framework (MOF)/hard-template/ionic-liquid multi-step procedures, thereby providing a strong basis for reproducible Fe–N 4 -like/Fe–N x oxidase-like nanozyme preparation and streamlined, robust bioanalysis.

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Acta Physiologica · 2026 ·Vol. 242 ·期 10 ·e70299 · IF 5.7

ITCH-Mediated Ubiquitination and Degradation of THBS1: A Key Mechanism for Enhancing Mitochondrial Biogenesis and Alleviating Mouse Skeletal Muscle Atrophy

Wan Yu,Yanteng Wang,Na Li,Difei Wang

Aim Skeletal muscle atrophy is tightly associated with maladaptive alterations in mitochondrial function and morphology. Itchy E3 ubiquitin-protein ligase (ITCH) modulates mitochondria, and thrombospondin 1 (THBS1) positively regulates muscle atrophy, but their roles in muscle atrophy are unclear. Methods A muscle atrophy model was established in C57BL/6 mice via daily intraperitoneal injection of dexamethasone (Dex, 20 mg/kg). ITCH overexpression in skeletal muscle was achieved by adeno-associated virus serotype 9 injection. C2C12 cells were treated with 50 μM Dex to mimic in vitro muscle atrophy. Skeletal muscle atrophy in mice was evaluated using hematoxylin–eosin staining and immunofluorescence staining. Mitochondrial damage was assessed via transmission electron microscopy, succinate dehydrogenase staining, and JC-1 staining. Immunoprecipitation-liquid chromatography/mass spectrometry, molecular docking, and co-immunoprecipitation were used to investigate the interaction between ITCH and THBS1. Phosphoproteomics analysis was performed to detect the THBS1 downstream proteins. Results Dex treatment downregulated ITCH expression in skeletal muscle. ITCH overexpression increased body weight, muscle mass, and muscle strength, downregulated the expression of atrophy-related genes (Atrogin-1, Mstn, MuRF-1), and promoted mitochondrial biogenesis. The results of the C2C12 cells were consistent with those obtained in vivo. Proteomic profiling and Co-IP confirmed ITCH–THBS1 interaction and subsequent THBS1 ubiquitination. THBS1 knockdown reduced the expression of Atrogin-1 and MuRF-1 and inhibited the phosphorylation of JUN and Map3k7, whereas THBS1 overexpression reversed the ITCH-mediated improvement in mitochondrial biogenesis. Conclusion ITCH enhances mitochondrial biogenesis and mitigates Dex-induced muscle atrophy by promoting the ubiquitin-dependent degradation of THBS1 and subsequent inhibition of downstream JUN/Map3k7 phosphorylation. Practitioner Points This study clarifies a novel regulatory mechanism of skeletal muscle atrophy, confirming that the E3 ubiquitin ligase ITCH plays a protective role in dexamethasone-induced muscle atrophy. THBS1 acts as a critical downstream effector of ITCH, promoting muscle atrophy via activation of the JUN/Map3k7 phosphorylation signaling pathway. Targeting ITCH-dependent THBS1 ubiquitination may represent a potential strategy to mitigate skeletal muscle loss.

CAS / MDL: 113775-47-6
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DIAMOND AND RELATED MATERIALS · 2025 · IF 5.1

Construction of MgFe2O4/rGO/WO3 Z-scheme photocatalyst for efficient degradation of organic pollutants: performance, mechanism, and reusability

Khanh-Huyen Nguyen,Thu-Hien Le,Thi-Duyen To,Xuan-Duc Nghiem,Dinh-Trinh Tran

MgFe 2 O 4 /rGO/WO 3 (MAG) Z -scheme visible light-driven photocatalyst was successfully synthesized with high purity. Synergic effects within MAG Z -scheme photocatalyst effectively enhanced the photocatalytic activity by a factor of 1.5–3.3. The photocatalytic performance was evaluated through the degradation of tetracycline (TC), ciprofloxacin (CIP) antibiotics, methylene blue (MB), direct blue 71 (DB-71), livestock and textile industrial wastewaters. MB and DB-71 degradation efficiency catalyzed by MAG reached 90.22 ± 2.56 % and 87.62 ± 2.26 % after 150 min, while these figures for TC and CIP were respectively 84.47 ± 2.16 % and 78.58 ± 2.36 %. The removal efficiency depended on contact time, pH value, catalyst dosage, pollutant concentration, and co-existing ions. Radical trapping tests and electron paramagnetic resonance spectroscopy analyses showed that superoxide anion radicals were mainly responsible for degrading the pollutants. The chemical oxygen demand and toxicology assessment revealed about 75 % of organic dyes and 67 % of antibiotics were mineralized while the toxicology of the by-products was negligible. The photocatalytic performance was high and stable after five repetitive cycles, with no discernible changes to the photocatalyst's surface properties. COD removal efficiency for textile and livestock wastewaters respectively reached 48.6 % and 42.9 %, lower than those for synthetic samples due to the presence of other organic compounds and co-existing ions, but met national technical regulations on the effluents of livestock and textile industry of Vietnam. The findings in this work provide a practical approach to mitigating hazardous organic dyes and antibiotics commonly found in textile and livestock wastewaters, thereby protecting public health and the environment.

CAS / MDL: 3317-61-1
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Advanced Healthcare Materials · 2025 · IF 9.6

Semiquinone Radical-Engineered Nanoparticles for Hypoxia-Adaptive and InflammationControlled Microwave-Immunotherapy of Liver Tumor

Meizhen Zhou,Jing Zhu,Dongyun Zhang,Jianping Dou,Wenqi Chen,Yi Zhang,Xiaopeng Gao,Jixi Zhang,Ping Liang,Jie Yu

Reactive Oxygen Species (ROS) exhibit a paradoxical dual role in tumor therapy. Tumor hypoxia restricts therapeutic ROS generation, while excessive secondary ROS post-ablation suppresses T-cell function yet promotes M1 macrophage polarization. Semiquinone radical-doped reduced polydopamine nanoparticles (PDA red ) loaded is developed with resiquimod (R848) (PDA red @R848) via π–π stacking. Reduction enriches the nanoparticles with semiquinone radicals, enhancing dielectric properties and dipole polarization under electromagnetic effects. This nanoparticle enables the specific hydrogen radicals (H•)/ROS generation in oxygen-heterogeneous tumor under microwave irradiation. In microwave dynamics therapy (MDT) phase, PDA red converts protons (H⁺) to H• under microwave irradiation in hypoxic regions, targeting cytochrome c and inducing tumor cell apoptosis and immunogenic cell death; PDA red establishes an internal electric field under microwave, facilitating electron–hole separation to produce ROS and trigger ferroptosis in normoxic regions. In post-MDT phase, PDA red ’s intrinsic polyphenols scavenge excess secondary ROS produced by damaged cells, alleviating immunosuppression. Compared with blank control, PDA red @R848 increased CD4⁺/CD8⁺ T-cell infiltration (6.4-fold) and M1 macrophage polarization (2.5-fold M1/M2 ratio elevation). Pro-inflammatory cytokines are significantly reduced, and tumor volume is suppressed by 94.8%. This study proposes an innovative dual-action mechanism coordinating oxygen-adapted radical generation with secondary ROS clearance to reprogram redox/immune homeostasis for effective liver tumor eradication.

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ACS Sensors · 2025 · IF 9.1

Phase-Sensitive Surface Plasmon Resonance Imaging with Polarization Modulation and Stokes Vector Measurement

Baiqi Cui,Xiaoyin Liu,Jinbiao Ma,Jingyu Wu,Yunxiao Wang,Haiying Ding,Di Wang,Qingjun Liu,Fenni Zhang

Phase-sensitive surface plasmon resonance (P-SPR) techniques offer superior sensitivity compared to conventional intensity-based SPR methods. However, current implementations, such as interference-based and polarization-based phase measurements, often face trade-offs between optical complexity and phase resolution, and typically lack access to full polarization information. Here, we report a compact and versatile Stokes vector-based polarization SPR imaging (Sp-SPRi) system that addresses these limitations through full Stokes vector analysis of imaging light after polarization modulation. This analysis enables the simultaneous acquisition of phase and multiple polarization parameters for enhanced molecular measurement. The Sp-SPRi system achieves a high phase sensitivity of 1.80 × 10–7 refractive index units (RIU), supporting kinetic, label-free detection and quantification of biomolecular interactions. We demonstrate its performance through kinetic measurements of protein binding, small molecule interactions, and in situ glycoprotein measurement of single cells. With its simplified optical configuration, microfluidic integration, and high-throughput imaging capabilities, Sp-SPRi provides a powerful platform for multidimensional biosensing. This work broadens the analytical scope of P-SPR, offering a robust and accessible approach for applications in point-of-care diagnostics, early disease detection, and drug screening.

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Biomedical Optics Express · 2023 ·Vol. 14 ·期 5 ·1862-1873 · IF 3.4

Fiber-integrated cantilever-based nanomechanical biosensors as a tool for rapid antibiotic susceptibility testing

Jie Zhou,Jie Zhou,Jiabin Huang,Jiabin Huang,Haoqiang Huang,Haoqiang Huang,Cong Zhao,Mengqiang Zou,Mengqiang Zou,Dejun Liu,Dejun Liu,Xiaoyu Weng,Liwei Liu,Junle Qu,Li Liu,Changrui Liao,Changrui Liao,Yiping Wang,Yiping Wang

There is an urgent need for developing rapid and affordable antibiotic susceptibility testing (AST) technologies to inhibit the overuse of antibiotics. In this study, a novel microcantilever nanomechanical biosensor based on Fabry–Pérot interference demodulation was developed for AST. To construct the biosensor, a cantilever was integrated with the single mode fiber in order to form the Fabry–Pérot interferometer (FPI). After the attachment of bacteria on the cantilever, the fluctuations of cantilever caused by the bacterial movements were detected by monitoring the changes of resonance wavelength in the interference spectrum. We applied this methodology to Escherichia coli and Staphylococcus aureus, showing the amplitude of cantilever’s fluctuations was positively related on the quantity of bacteria immobilized on the cantilever and associated with the bacterial metabolism. The response of bacteria to antibiotics was dependent on the types of bacteria, the types and concentrations of antibiotics. Moreover, the minimum inhibitory and bactericidal concentrations for Escherichia coli were obtained within 30 minutes, demonstrating the capacity of this method for rapid AST. Benefiting from the simplicity and portability of the optical fiber FPI-based nanomotion detection device, the developed nanomechanical biosensor in this study provides a promising technique for AST and a more rapid alternative for clinical laboratories.

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Inorganic Chemistry Frontiers · 2023 ·Vol. 10 ·期 14 ·4045-4053 · IF 7

A mixed-valence biotinylated Cu(I/II) complex for tumor-targeted chemodynamic therapy accompanied by GSH depletion

Zhaoguo Hong,Xin You,Jingjing Zhong,Di Yao,He-Dong Bian,Shulin Zhao,Liangliang Zhang,Hong Liang,Fu-Ping Huang

Chemodynamic therapy (CDT), in which highly toxic hydroxyl radicals (˙OH) could be triggered by a Fenton or Fenton-like reaction to kill cancer cells, has emerged recently. Compared to traditional CDT nanomaterials, herein, an atomically-precise biotinylated Cu(I/II) complex [CuICuIICl2(VBio)]·CH3OH (VBio = deprotonated O-vanillin biotinylhydrazone), denoted VBio-CuICuII, was rationally designed and synthesized successfully. This targeted Fenton-like agent, VBio-CuICuII, is constructed from a hydroxyl radical-producible CuI ion, a CuII center as a GSH depletor for an augmented CDT effect, and a biotin moiety as a cancer-targeting unit. Owing to the obvious cell selectivity discrepancy of biotin towards normal and cancerous cells, VBio-CuICuII was able to preferentially accumulate in tumor cells. Meanwhile, the CuI metal center could be used as a Fenton-like agent to generate ˙OH. Furthermore, the CuII in VBio-CuICuII was available for successive ˙OH production via a CuI/CuII-circulation strategy under a GSH-rich tumor site, thereby improving catalytic efficiency. More importantly, in vivo results further demonstrate that VBio-CuICuII could significantly inhibit tumor growth without obvious damage toward major organs. Therefore, this multiple-identity Fenton-like agent could provide an appreciable reference value for the design of atomically precise CDT agents.

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DRUG DELIVERY · 2023 · IF 6

Paclitaxel-loaded ROS-responsive nanoparticles for head and neck cancer therapy

Yaqin Tu,Wei Zhang,Guorun Fan,Chenming Zou,Jie Zhang,Nan Wu,Jiahui Ding,Wen Qing Zou,Hongjun Xiao,Songwei Tan

High intracellular reactive oxygen species (ROS) level is characteristic of cancer cells and could act as a target for the efficient targeted drug delivery for cancer treatment. Consequently, biomaterials that react to excessive levels of ROS are essential for biomedical applications. In this study, a novel ROS-responsive polymer based on D-α-Tocopheryl polyethylene glycol 1000 succinate (TPGS) and poly (β-thioester) (TPGS-PBTE) was synthesized for targeted delivery of the first-line antineoplastic drug, paclitaxel (PTX). The resultant TPGS-PBTE NPs showed good ROS-responsive capability in size change and drug release. Compared to PTX, PTX-loaded nanoparticles (PTX@TPGS-PBTE NPs) showed enhanced cytotoxicity and higher level of apoptosis toward squamous cell carcinoma (SCC-7) cells. Tumor-targeted delivery of the NPs was also observed, especially after being modified with a tumor-targeting peptide, cRGD. Enhanced tumor growth inhibition was also observed in head and neck cancer SCC-7 murine models. In summary, PTX@TPGS-PBTE NPs can achieve good therapeutic effects of PTX against head and neck cancer both in vitro and in vivo, especially when modified by cRGD for active targeting, which enriched the application of ROS responsive system utilized in the delivery of anticancer drugs.

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JOURNAL OF CONTROLLED RELEASE · 2023 · IF 10.8

Modulating tumor-stromal crosstalk via a redox-responsive nanomedicine for combination tumor therapy

Yuxin Zhang,Jie Zhou,Xiaoting Chen,Zhiqian Li,Lei Gu,Dayi Pan,Xiuli Zheng,Qianfeng Zhang,Rongjun Chen,Hu Zhang,Qiyong Gong,Zhongwei Gu,Kui Luo

Interaction between carcinoma-associated fibroblasts (CAFs) and tumor cells leads to the invasion and metastasis of breast cancer. Herein, we prepared a redox-responsive chondroitin sulfate (CS)-based nanomedicine , in which hydrophobic cabazitaxel (CTX) was conjugated to the backbone of CS via glutathione (GSH)-sensitive dithiomaleimide (DTM) to form an amphipathic CS-DTM-CTX (CDC) conjugate, and dasatinib (DAS) co-assembled with the CDC conjugate to obtain [email protected] After CD44 receptor-mediated internalization by CAFs, the nanomedicine could reverse CAFs to normal fibroblasts, blocking their crosstalk with tumor cells and reducing synthesis of major tumor extracellular matrix proteins , including collagen and fibronectin . Meanwhile, the nanomedicine internalized by tumor cells could effectively inhibit tumor proliferation and metastasis, leading to shrinkage of the tumor volume and inhibition of lung metastasis in a subcutaneous 4T1 tumor model with low side effects. Collectively, the nanomedicine showed a remarkably synergistic therapy effect against breast cancer by modulating tumor-stromal crosstalk.

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FOOD CHEMISTRY · 2023 · IF 8.8

Exploring inhibitory effect and mechanism of hesperetin-Cu (II) complex against protein glycation

Xi Peng,Xing Hu,Kai Liu,Deming Gong,Guowen Zhang

Inhibition of advanced glycation end products (AGEs) formed in protein glycosylation is crucial for minimizing diabetic complications. Herein, the anti-glycation potential of hesperetin-Cu (II) complex was investigated. Hesperetin-Cu (II) complex strongly inhibited three stages glycosylation products in bovine serum albumin (BSA)-fructose model, especially for the inhibition of AGEs (88.45%), which was stronger than hesperetin (51.76%) and aminoguanidine (22.89%). Meanwhile, hesperetin-Cu (II) complex decreased the levels of BSA carbonylation and oxidation products. 182.50 µg/mL of hesperetin-Cu (II) complex inhibited 66.71% β-crosslinking structures of BSA, and scavenged 59.80% superoxide anions and 79.76% hydroxyl radicals. Moreover, after incubating with methylglyoxal for 24 h, hesperetin-Cu (II) complex removed 85.70% methylglyoxal. The mechanisms of protein antiglycation by hesperetin-Cu (II) complex may be through protecting structure, trapping methylglyoxal, scavenging free radicals and interacting with BSA. This study may contribute to the development of hesperetin-Cu (II) complex as a functional food additive against protein glycation.

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