Nanoscale Horizons
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2026
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IF 6.4
Ning Ding,Qing Yu,Ziyuan Su,Yiting Han,Yajuan Chang,Dongzhi Yang,Shuai Cui,Xu Wang
Suboptimal reactive oxygen species (ROS) production in photodynamic therapy (PDT) and chemodynamic therapy (CDT) due to tumor antioxidants and H2O2 constraints poses a challenge to their therapeutic efficacy. To address this, our study introduces GOx@MPN@Gel, a novel PDT/CDT platform that integrates glucose oxidase (GOx), luteolin, iron ions, a traditional Chinese medicine-inspired metal-phenolic network (MPN), and hydrogel (Gel) carriers to enhance ROS generation. Experimental results demonstrate GOx@MPN@Gel heightened acid sensitivity, robust GOx activity, and significant ROS production. Both in vitro and in vivo tests validate its therapeutic potential. Within the tumor microenvironment, GOx@MPN@Gel effectively elevates H2O2 levels for CDT, producing cytotoxic hydroxyl radicals (·OH), and upon near infrared (NIR) light exposure, its porphyrin component triggers potent PDT effects, generating additional ROS. This synergistic approach significantly enhances antitumor efficacy. The platform's unique design, combining acid-responsive degradation and PDT/CDT synergy, offers a promising personalized treatment strategy for breast cancer.
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PubMed
高影响因子
JOURNAL OF NANOBIOTECHNOLOGY
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2026
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IF 15
Tang Honglin,Wu Chongzhi,Wang Wei,Cheng Xi,Dong Yong,Gao Zhiyuan,Chen Pengfei,Xie Xin,Huang Yong,Sun Lihe,Li Bowen,Li Da
Ferroptosis, an iron-dependent form of regulated cell death driven by lipid peroxidation (LPO), has emerged as a promising strategy for cancer therapy but remains limited by insufficient hydrogen peroxide (H₂O₂), restricted catalytic iron availability, and the extremely short lifetime of hydroxyl radicals (·OH) in the tumor microenvironment. Here, we report a self-assembled nano-prodrug designed to amplify oxidative stress through coordinated reactive oxygen species (ROS)-reactive nitrogen species (RNS) cascades. Transcriptomic analyses of melanoma cohorts revealed that the redox enzyme NAD(P)H: quinone oxidoreductase-1 (NQO1) is frequently upregulated and associated with oxidative stress and ferroptosis-related transcriptional programs, suggesting a potential redox vulnerability that can be therapeutically exploited. Guided by this observation, a glutathione-responsive nanoplatform (HFSAL) was constructed from a disulfide-bridged ferrocene–arginine scaffold (Fc-SS-Arg) with β-lapachone (β-lapa) co-loaded and hyaluronic acid coating for tumor-targeted delivery. Upon intracellular activation, β-lapa undergoes NQO1-mediated redox cycling to generate H₂O₂, which is further converted into ·OH through ferrocene-catalyzed Fenton reactions. Meanwhile, arginine-derived nitric oxide (NO) reacts with ROS intermediates to form highly reactive peroxynitrite (ONOO⁻), thereby amplifying oxidative damage and extending the effective range of redox stress. In addition, NO-mediated vascular remodeling alleviates tumor hypoxia and enhances intratumoral drug accumulation. Consequently, the HFSAL nano-prodrug effectively induces synergistic ferroptosis and apoptosis, leading to significant tumor growth inhibition and metastasis suppression in vivo with favorable biosafety. This work presents a redox-amplifying nano-prodrug strategy that exploits NQO1-associated metabolic vulnerability to enhance ferroptosis-based cancer therapy. Graphical
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高影响因子
CHEMICAL ENGINEERING JOURNAL
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2026
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IF 12.5
Ping Li,Lu Yang,Yifei Song,Shanshan Li,Wenhong Zheng,Mengteng Tang,Guoyang Xu,Wei Feng,Li-Li Li
Chronic refractory wounds in diabetic patients pose a substantial clinical challenge owing to fluctuating pH levels, bacterial infections, and compromised healing mechanisms. Here, we have developed a metabolic dynamic self-adaptive cobalt-based hydrogel dressing that incorporates spatially confined biomineralized enzyme (glucose oxidase) nanoflowers with high catalytic efficiency and a polyvinylpyrrolidone (PVP) hydrogel matrix with superior unidirectional water absorption capacity. The elevated glucose metabolism in diabetic wounds was harnessed to enable efficient cascade catalysis to convert glucose into hydrogen peroxide (H 2 O 2 ), followed by Co 2+ /Co 3+ redox reactions that sustain spatiotemporal reactive oxygen species (ROS) generation. The low redox potential of the cobalt hydrogel allows robust catalytic activity (>75%) across a wide pH range (4.0–9.0) for over 50 h to adapt to the entire process of wound repair. Moreover, the hydrogel reduces the diffusion distance between ROS and bacteria, resulting in potent broad-spectrum antibacterial activity, including biofilm eradication, against multidrug-resistant Escherichia coli , Pseudomonas aeruginosa , and methicillin-resistant Staphylococcus aureus (MRSA). In an immunosuppressed mouse model of diabetic trauma, it was demonstrated that under hyperglycemic conditions, the GCP hydrogel facilitated a wound closure rate of 97.4% by day 12. Our strategy paves the way for the development of advanced intelligent wound dressings featuring dynamic, self-adaptive microenvironments and persistent antimicrobial activity.
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高影响因子
JOURNAL OF NANOBIOTECHNOLOGY
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2026
·Vol. 24
·期 1
·250
·
IF 15
Zhu Jiankang,Zhang Yun,Li Bingjun,Jin Xin,Liu Chuxuan,Li Linchuan,Li Luyu,Zhang Hongyu,Zhang Guangyong
Background High reactive oxygen species (ROS) concentration displays dual functions, potentially promoting both tumor cell death and driving tumor-associated macrophage (TAM) polarization towards the M1-type to elicit a series of antitumor immune responses, positioning ROS as ideal tumor therapeutic molecules. However, sustained efficacy and precise ROS targeting at tumor sites retains numerous challenges. In this study, we present the synthesis of a nanoplatform, ZIF-8@XOR, comprising Xanthine oxidoreductase (XOR) with high intracellular enzymatic activity for high-level ROS generation and ZIF-8, a versatile zeolite imidazolate framework-8 carrier with high tumor site loading and targeting efficiency. Results: Our results revealed that ZIF-8@XOR targets tumor cells and elicits intracellular ROS both in vitro and in vivo, inducing tumor cell death. Moreover, intracellular ROS elicitation in TAM supports macrophage polarization towards the M1-type. In vivo, tumor-associated antigen pool generation from ROS-induced apoptosis of tumor cells further stimulates increased infiltration and macrophage activation in the tumor microenvironment. This, in turn, leads to increased tumor infiltration of CD8 + T cells with a cytokine profile, indicating cytotoxic effects and suggesting a successfully induced adaptive anti-tumor response. Conclusion: The hereby-presented newly developed nanomaterial could serve as a promising novel tool for gastric cancer immunotherapy. Graphical
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ADVANCED FUNCTIONAL MATERIALS
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2026
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IF 19.9
Shuo Qiu,Yundi Wu,Ruocan Liu,Huanran Qu,Shiyang Shao,Jianqiang Chen,Xilong Wu
Reactive oxygen species (ROS)-based therapies are promising for tumor ablation, but their efficacy is limited by hypoxic microenvironments and poor intratumoral penetration. This study presents a photo/sono/magneto-responsive ternary heteronanocrystal, BPNS/PCN-224/Fe 3 O 4 @PVP (BPF), incorporating an S-scheme heterojunction and Fe-based nanozyme catalysis. The S-scheme heterojunction between piezoelectric black phosphorus nanosheets (BPNS) and photosensitizing PCN-224 enhances ROS generation for synergistic photodynamic therapy (PDT) and ultrasound-piezocatalytic therapy (UPCT). Superparamagnetic Fe 3 O 4 nanoparticles provide peroxidase- and catalase-like activities, further increasing oxidative stress and reinforcing PDT, UPCT, and chemodynamic therapy. This robust ROS production induces immunogenic cell death, activates immune memory, and elicits systemic antitumor responses. Under ultrasound and magnetic driving, BPF is enriched and actively transported into deep tumor regions, improving intratumoral distribution. The integrated platform achieves efficient ROS-amplified tumor cell killing, along with near-infrared fluorescence and T 2 -weighted MRI for real-time treatment guidance. This multifunctional S-scheme heteronanocrystal offers a promising strategy for penetrative, ROS-amplified tumor ablation, and enhancing systemic antitumor immune responses.
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Regenerative Biomaterials
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2026
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IF 8.7
Zhang Renjie,Jia Qingqing,Wang Jiahao,Li Wei,Chen Jiang,Hong Wenxin,Huang Huiying,Lin Quankui
Cataract is the leading cause for blindness. While the intraocular lens (IOL) implantation is the only effective treatment in cataract surgery. Posterior capsule opacification (PCO) is the most frequent complication after cataract surgery, mainly resulting from the proliferation and migration of residual human lens epithelial cells (HLECs) within the capsular bag. While surface modification of IOL has helped slow its progression, long-term effectiveness and biocompatibility remain major challenges. Supraphysiological concentration of reactive oxygen species (ROS) induced by natural enzyme stimulation can effectively inhibit proliferation and migration of HLECs, but the effect is limited by enzyme instability. Gold nanoparticles (AuNPs), a promising candidate with enzyme-mimicking activity and desirable photothermal effects, can promote ROS generation and enhance cell apoptosis. To prevent AuNPs aggregation, Fe3+ containing MIL metal-organic frameworks (MOFs) were used as a supporting framework to obtain AuNPs@MIL, which was then modified onto IOL material via electrostatic layer by layer (LbL) self-assembly technique to improve stability and increase immobilization efficiency. The cascade catalytic process, initiated by AuNPs@MIL, can catalyze glucose and oxygen oxidation to produce gluconic acid and hydrogen peroxide. In the formed acidic environment, AuNPs, along with Fe3+ from MIL, convert H2O2 into ·OH via oxidase-like and Fenton-type reactions, which will accelerate cell apoptosis. Additionally, NIR-induced photothermal therapy (PTT) of AuNPs further eliminates abnormally proliferating cells. In vitro and in vivo studies demonstrate that AuNPs@MIL modified IOL offers effective PCO prevention effect, good biocompatibility and excellent optical properties, presenting a viable solution for long-term, efficient PCO prevention.
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高影响因子
Biomaterials Science
·
2026
·
IF 6.1
Qi Zhang,Luyao Wang,Zhaofan Yang,Hao Meng,Shixian Lv,Linlin Liu
Chemo-immunotherapy aims to integrate chemotherapy-induced antigen release with innate immune activation to achieve enhanced antitumor efficacy. However, the pharmacokinetic mismatch and systemic toxicity of free small molecules often compromise the synergistic effects. Herein, we propose a reactive oxygen species (ROS)-responsive nanoplatform based on mPEG–PCL for the co-delivery of a paclitaxel (PTX) prodrug and the TLR7/8 agonist R848. The nanoparticles remain stable under physiological conditions while releasing drug in oxidative tumor microenvironments, thereby achieving synchronous intratumoral delivery and activation. In vitro, the system exhibited efficient intracellular uptake and potent cytotoxicity against tumor cells while maintaining low toxicity toward normal cells due to prodrug design. Moreover, the platform effectively induced immunogenic cell death and promoted dendritic cell maturation, highlighting its capacity for chemo-immunotherapeutic synergy. This co-delivery strategy provides a versatile approach to realize controllable and safe chemo-immunotherapy through stimuli-responsive nanomedicine design.
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高影响因子
BIOMACROMOLECULES
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2026
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IF 5.9
Xiaopeng Cheng,Yexin Li,Jiuhao Zhou,Shanfeng Wang
Abstract Here we present our systematic investigation on how thiols and reactive oxygen species (ROS) affect the de-crosslinking behavior and thermal properties of sulfur-based covalent adaptive networks (CANs) prepared with novel photo-crosslinkable poly(ε-caprolactone) lipoates (PCLLAs). By integrating experimental data with the Flory-Rehner theory, we reveal the distinctions between the two de-crosslinking degradation processes in terms of crosslinking density, gel fraction, swelling ratio, and their impact on the thermal and antioxidant properties of PCLLA networks. Thiols in good solvents rapidly and reversibly cleave disulfide crosslinks to sharply reduce the crosslinking density and to enhance chain mobility, leading to increased melting point (Tm) and unchanged crystallinity of the network. Dynamic mechanical analysis further showed that thiol-induced de-crosslinking progressively reduced high-temperature storage modulus retention while increasing viscous dissipation. In contrast, ROS in aqueous solutions can cause slow and irreversible oxidative scission of disulfide bonds in the networks, resulting in increases in both Tm and crystallinity. The 3D printability of PCLLAs and the intrinsic antioxidant activity of the networks are also demonstrated. This study shows that the de-crosslinking kinetics and material properties of sulfur-based CANs can be efficiently tuned by regulating the de-crosslinking pathways, providing a strategy for designing degradable, stimuli-responsive, and functionally programmable polymer networks.
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高影响因子
JOURNAL OF NANOBIOTECHNOLOGY
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2026
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IF 15
Mengmeng Dong,Xiaomin Huang,Kaiqiang Li,Xiaorong Zhu,Tingting Hu,Xiaohuan Guo,Ke Hao,Fei Kong,Mei Yang,Ning Hu,Yingwei Wang,Lisen Lu,Zhen Wang
Acetaminophen (APAP) induced acute liver injury (ALI) is driven by a self amplifying cascade of reactive oxygen species (ROS) and lipid peroxidation, yet current therapies fail to interrupt this pathological loop. Here we engineer a liver targeted hierarchical nanozyme, SOD@ZIF-8/Mn 3 O 4 , which integrates natural superoxide dismutase (SOD) and Mn 3 O 4 nanozymes within a ZIF‑8 nanoplatform. Unlike conventional single step scavengers, this system implements a catalytic hierarchy matching strategy. SOD rapidly converts O 2 · − to H 2 O 2 , while Mn 3 O 4 simultaneously decomposes H 2 O 2 and intercepts ·OH, thereby converting the entire ROS cascade into benign water. Density functional theory calculations reveal that the SOD–Mn 3 O 4 interface lowers the energy barriers for catalase like and glutathione peroxidase like steps, establishing a synergistic channeling effect. In APAP injured AML-12 cells and a murine ALI model, the nanozyme not only alleviates oxidative stress and lipid peroxidation but also breaks the ROS inflammation feed forward loop by restoring the Keap1/Nrf2/HO‑1 redox switch and suppressing NF‑κB activation. Transcriptomic and functional analyses confirm that treatment rewires hepatic transcriptional programs associated with lipid metabolism and inflammatory signaling. This work establishes a modular nanozyme natural enzyme hybrid platform where the MOF acts as a spatiotemporal organizer, transforming the pathological ROS chain into a controlled detoxification pathway. The concept is readily extensible to other diseases driven by sequential ROS cascades, offering a paradigm shift from single enzyme mimicry to pathway reprogramming nanobiocatalysis.
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PubMed
高影响因子
ADVANCED FUNCTIONAL MATERIALS
·
2026
·
IF 19.9
Junyuan Zhang,Tong Zhou,Jiwei Sun,Baoying Zhao,Huaibin Yu,Chengchen Wu,Haoqi Lei,Yifan Zhang,Yang Liu,Yifan Wang,Zhicai Feng,Yuzhou Wu,Cheng Yang
Excessive reactive oxygen species (ROS) accumulation, cartilage matrix degeneration, and impaired lubrication are central drivers of osteoarthritis (OA). However, poor matrix retention limits drug delivery to chondrocytes and lubrication restoration. Here, we develop a zwitterion-based, thioketal-crosslinked Superoxide Dismutase (SOD)-polymer complex (SOD-SADT) via in situ atom transfer radical polymerization, in which polymers grow from the enzyme surface and envelop SOD to form a nanoscale cocoon. The polymer shell exhibits cartilage-matrix affinity through van der Waals and electrostatic interactions with type II collagen and chondroitin sulfate. Accordingly, its zwitterionic hydration layer enables matrix-anchored lubrication, substantially reducing the coefficient of friction of OA-like cartilages. Meanwhile, SOD-SADT establishes a chem-bio coupling for ROS elimination that couples enzymatic·O 2 − dismutation with thioketal-triggered chemical depletion of H 2 O 2 and·OH, achieving up to ∼80% ROS scavenging. Notably, SOD-SADT achieves high chondrocyte uptake (∼ 91.7 ± 3.4%) and promotes lysosomal escape. This enhances intracellular utilization, thereby attenuating oxidative injury and restoring anabolic/catabolic balance. In a mouse model of OA, intra-articular SOD-SADT preserves cartilage structure and improves joint function, thereby markedly slowing OA progression. Overall, this work offers a dual-action strategy that couples intracellular antioxidant regulation with extracellular lubrication repair to address OA.
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高影响因子
JOURNAL OF DRUG DELIVERY SCIENCE AND TECHNOLOGY
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2026
·
IF 5.2
Jian Yang,Mingjuan Xu,Yanzhu Li,Wei Su,Yao Qian,Jun Yi
Knee osteoarthritis (KOA) is a degenerative joint disorder characterized by excessive reactive oxygen species (ROS) accumulation, persistent inflammation, and progressive extracellular matrix (ECM) degradation. However, effective modulation of the pathological redox-inflammatory microenvironment remains challenging due to the poor bioavailability of natural antioxidants and the limited catalytic durability of conventional nanomaterials. In this study, we report a polyethylene glycol (PEG)-assisted coordination assembly strategy to construct an osthole–ceria (OST–CeO 2 ) nanocomposite with synergistic ROS-scavenging and chondroprotective functions. The resulting OST-CeO 2 nanoparticles exhibit a uniform quasi-spherical morphology, a hydrodynamic diameter of 150 nm, a mildly positive surface charge, excellent colloidal stability, and pH/ROS dual-responsive release profiles. In vitro assays confirm that OST-CeO 2 possesses potent concentration-dependent antioxidant activity against diverse radicals including DPPH·, ABTS + ·, and hydrogen peroxide. In IL-1β-stimulated ATDC5 chondrocytes, OST-CeO 2 treatment restores cell viability and significantly suppresses pro-inflammatory cytokines (IL-1β, TNF-α, IL-6). In an H 2 O 2 -induced oxidative stress model, it effectively quenches intracellular ROS, reinstates antioxidant enzyme activities such as superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx), and reduces malondialdehyde (MDA) levels. Furthermore, intra-articular injection of OST-CeO 2 in a destabilization of the medial meniscus (DMM)-induced KOA mouse model significantly attenuates cartilage erosion, lowers Mankin and OARSI histological scores, and improves joint function, with no appreciable toxicity to major organs. Collectively, OST-CeO 2 integrates ceria-mediated catalytic ROS elimination with osthole's inherent antioxidant and anti-inflammatory properties, establishing a dual-functional nano-antioxidant platform that reshapes the redox and inflammatory imbalance in the KOA niche. This study presents a promising nanotherapeutic strategy for cartilage preservation and provides a foundation for designing hybrid systems combining natural bioactive compounds with nanozymes against degenerative joint diseases. Download: Download high-res image (294KB) Download: Download full-size image
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高影响因子
Materials Today Bio
·
2026
·
IF 11
Rujing Wang,Lan Zou,Dandan Mi,Chuan Wang,Zijian Song,Tiantian Liu,Mengnan Zhao,Dong Wang,Sanjun Shi
Tumor metastasis, a leading cause of cancer-related mortality, presents a significant challenge due to its complex, multi-step nature and tumor cells’ adaptability. Current targeted therapies often face limitations as tumor cells activate compensatory signaling pathways, leading to drug resistance. Here, we introduce a novel molecular drug pair of sorafenib (Sora) and curcumin (Cur) self-assembled into Sora-Cur@diploid nanoparticles (diNPs), which were transformed into label-free diNP@pharmaceutical dots (diNP@PDs) with enhanced fluorescence through a specialized formulation process, eliminating the need for chemical modification. diNP@PDs exhibit photoluminescence capability, simultaneously promoting cross-talk among lysosomes, mitochondria, and nuclei. This lysosomes-mitochondria-nuclei interaction induces perinuclear clustering of organelles, triggering nuclear reactive oxygen species (nuROS) generation. The nuROS epigenetically suppresses HDAC2 activity, inhibiting epithelial-mesenchymal transition (EMT) and tumor metastasis. By integrating multi-organelle targeting with molecular therapy, diNP@PDs offer an innovative strategy for both imaging and inhibiting tumor metastasis, highlighting the potential of interorganelle approaches in oncology. Download: Download high-res image (351KB) Download: Download full-size image
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