JOURNAL OF NANOBIOTECHNOLOGY纳米生物技术杂志
JOURNAL OF NANOBIOTECHNOLOGY(英文缩写 J NANOBIOTECHNOL),ISSN 1477-3155,eISSN 1477-3155,中文译名:纳米生物技术杂志 是一本学术期刊。本页汇总该期刊的最新影响因子、分区信息以及最新收录于 PubMed 的文献,帮助您快速了解期刊全貌。
发文量统计区间：2025-11-01 至 2026-10-31，按本站收录文献的发表日期统计。
期刊介绍
JOURNAL OF NANOBIOTECHNOLOGY 最新收录文献
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1. {"_":"Ultrasound-activated CuSe/TiO heterostructured nanosonosensitizer enables coordinated induction of ferroptosis and cuproptosis for tumor immunotherapy.","sub":["2-X","2"]}
PMID:日期:2026-09-27Triple-negative breast cancer (TNBC) is a highly aggressive subtype characterized by the absence of actionable molecular targets, high metastatic propensity, and limited responsiveness to current immunotherapies. Although immune checkpoint inhibitors show promise, their clinical efficacy is constrained by low tumor immunogenicity and a highly immunosuppressive tumor microenvironment (TME). This study reports a hyaluronic acid (HA)-functionalized TiO@Cu-Se@HA nanosystem that promotes the coordinated induction of ferroptosis and cuproptosis, thereby enhancing sonodynamic immunotherapy against TNBC. It features a rationally designed Cu-Se/TiO heterostructured nanosonosensitizer and an integrated therapeutic strategy combining ultrasound-activated sonodynamic effects with the coordinated induction of ferroptosis and cuproptosis. Under ultrasound irradiation, the Cu-Se/TiO heterointerface promotes efficient electron transfer and reactive oxygen species (ROS) generation, markedly amplifying sonodynamic efficacy. Meanwhile, released Cu depletes intracellular glutathione, disrupts redox homeostasis, thereby promoting copper-dependent proteotoxic stress. In parallel, Cu induces autophagic degradation of glutathione peroxidase 4, further enhancing ferroptotic signaling. This coordinated induction effectively suppresses tumor growth, remodels the immunosuppressive TME, and potentiates antitumor immunity, as further corroborated by single-cell RNA sequencing. Collectively, this study provides a rational strategy for integrating sonodynamic therapy with dual non-apoptotic cell death pathways, offering a promising strategy to sensitize TNBC to immunotherapy.
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2. Tumor cell membrane‑coated MOF‑199 nanoparticles co‑loaded with auranofin and celecoxib enhance single‑dose radiotherapy and anti‑PD‑L1 therapy in cervical cancer.
2. 肿瘤细胞膜包覆的MOF-199纳米颗粒共载金诺芬和塞来昔布增强宫颈癌单剂量放疗和抗PD-L1治疗PMID:日期:2026-09-25Cervical cancer (CC) remains one of the leading causes of cancer-related death among women worldwide. Radiotherapy (RT) is an integral component of multimodal treatment for CC. Beyond its direct cytotoxic effects mediated by radiation-induced DNA damage, RT can also elicit antitumor immunity by promoting the generation of reactive oxygen species (ROS) and inducing immunogenic cell death (ICD). This immunomodulatory property provides a strong rationale for combining RT with immune checkpoint inhibitors (ICIs), a combination strategy that holds promise for enhancing therapeutic efficacy in CC. However, CC cells can exploit their antioxidant defense systems to counteract the oxidative stress induced by RT. The glutathione (GSH) and thioredoxin 1 (Trx1) antioxidant systems constitute the major intracellular antioxidant barriers of CC. They can attenuate ICD by scavenging ROS to limit RT-induced antitumor immune activation, thereby diminishing the efficacy of RT and ICIs combination treatment. Additionally, RT can also activate cyclooxygenase-2 (COX-2) to promote the production and release of prostaglandin E2 (PGE2), in turn suppressing DC maturation, consequently weakening ICD-mediated activation of anti-tumor immunity. Hence, we herein designed a tumor cell membrane-coated copper-based metal-organic framework nanomaterial (MOF-199) co-delivering auranofin and celecoxib (MAC@M) for co-targeting the antioxidant system and COX-2/PGE2 pathway to augment radioimmunotherapy efficacy in CC. In vitro experiments demonstrated that MAC@M could significantly enhance RT to increase CRT exposure, HMGB1 release, and ATP secretion, as well as promote DC activation. In animal models, MAC@M combined with RT elicited robust CD8⁺ T cell and NK cell-mediated antitumor immune responses, which largely contributed to local tumor control and a pronounced systemic antitumor effect, ultimately improving ICI efficacy in CC. Collectively, our study may provide a new combinatorial treatment strategy against CC.
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3. Retraction Note: Liposome-lentivirus for miRNA therapy with molecular mechanism study.
3. 撤稿说明：用于miRNA治疗的脂质体-慢病毒及其分子机制研究PMID:日期:2026-09-15该文献暂无摘要。
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4. Visualized self-propelled nanorobots overcome tumor barriers for boosted photothermal-nanocatalytic synergistic therapy against triple-negative breast cancer.
4. 可视化自驱动纳米机器人克服肿瘤屏障以增强光热-纳米催化协同治疗三阴性乳腺癌PMID:日期:2026-09-14Conventional nanozyme-based therapeutics for triple-negative breast cancer (TNBC) are severely hindered by insufficient tumor penetration and lysosomal degradation-induced enzyme inactivation, crippling therapeutic efficacy. Herein, we rationally construct visualized dual-propelled Janus PDAPdAu nanorobots (PPA NBs) with cascade catalytic activity for synergistic photothermal-nanocatalytic therapy of TNBC. Powered by near-infrared light-triggered thermophoresis and nanozyme-fueled oxygen propulsion, PPA NBs realize deep tumor penetration and lysosomal escape. PPA NBs exhibit catalase-mimicking activity to alleviate tumor hypoxia through hydrogen peroxide decomposition, and glucose oxidase-mimicking activity to deplete glucose and downregulate heat shock proteins, thus sensitizing TNBC to photothermal therapy (PTT). Localized hyperthermia further enhances nanozyme catalysis, forming an amplified synergy between nanocatalytic therapy and PTT that affords an outstanding 97% tumor inhibition rate. Furthermore, PPA NBs act as excellent fluorescent biosensing probes for visual lesion localization. Overall, this work provides visual diagnosis and advanced TNBC phototherapy strategies, a reliable paradigm for cancer patients' health monitoring and treatment.
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5. Publisher Correction: Human umbilical cord-derived mesenchymal stem cell exosomes ameliorate hepatocyte ferroptosis and sepsis-associated liver injury by restoring iron homeostasis in hepatocytes.
5. 出版商更正：人脐带间充质干细胞外泌体通过恢复肝细胞铁稳态改善肝细胞铁死亡和脓毒症相关肝损伤PMID:日期:2026-09-09该文献暂无摘要。
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6. Sprayable hydrogel loaded with engineered fusion cellular vesicles for cancer recurrence suppression.
6. 负载工程化融合细胞囊泡的可喷雾水凝胶用于抑制癌症复发PMID:日期:2026-09-07Surgical resection often leaves residual lesions that lead to tumor recurrence and high mortality across various cancer types, a challenge that is particularly pronounced in oral squamous cell carcinoma. Herein, we developed a sprayable hydrogel loaded with fusion cellular vesicles (Fus-CVs) and characterized its structural and mechanical properties for the prevention of postoperative tumor recurrence. Fus-CVs co‑express PD‑1 to engage PD‑L1 on tumor cells and CD36 to competitively bind oxidized lipids in the tumor microenvironment, thereby effectively reversing T cell exhaustion and restoring T cell effector function. Additionally, the sprayable hydrogel, formed by crosslinking sodium alginate (SA) with the ionic solution (calcium chloride, CaCl; manganese chloride, MnCl), enables sustained local delivery of Fus‑CVs to potentiate T cell‑mediated killing of residual tumor cells. In vitro experiments and primary tumor model confirmed that Fus‑CVs specifically achieve dual targeting of PD-L1 on tumor cells and oxidized lipids in the tumor microenvironment, reverse T cell exhaustion and achieve combination therapy. In an established postoperative recurrence mouse model, the SA solution containing Fus-CVs and the ionic solution could be co-sprayed to rapidly form a conformal, uniform and stable layer on irregular tissue surfaces, enabling sustained local release of Fus-CVs and achieve effective tumor recurrence suppression. Fus‑CVs-loaded sprayable hydrogel not only achieves dual functionality in immune checkpoint blockade and lipid metabolic regulation but also offers localized controlled release, and reduced systemic toxicity, thereby presenting a clinically translatable strategy for postoperative recurrence prevention.
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7. A CD44-targeted PDA/ZnO redox-active nanocomposite that couples chemotherapy with mitochondrial stress and tumor immune remodeling.
7. 一种靶向CD44的PDA/ZnO氧化还原活性纳米复合材料，将化疗与线粒体应激和肿瘤免疫重塑相结合PMID:日期:2026-09-05Bladder cancer therapy is frequently limited by inefficient drug retention and adaptive immune resistance within a hypoxic tumor microenvironment. Here, we report a CD44-targeted, fully synthetic nanocomposite (HPPZC) that converts chemotherapy into a mitochondria-associated therapeutic strategy accompanied by tumor immune remodeling. Rapid microwave-assisted assembly integrates hyaluronic acid (HA), polydopamine (PDA), protamine, zinc oxide (ZnO), and camptothecin (CPT) into a structurally integrated hybrid nanocomposite with tumor targeting, while the PDA/ZnO interface functions as a redox-active platform associated with mitochondrial dysfunction and redox modulation. HPPZC induces rapid mitochondrial depolarization, elevates oxidative stress, and is associated with PINK1/Parkin-related mitochondrial quality-control and autophagy-associated turnover signatures. In vivo, HPPZC treatment prolonged local intratumoral retention and produced tumor regression. The combination of chemotherapy with mitochondrial stress and tumor immune remodeling, suppressing CXCL12 and PD-L1, promoting M1-like marker profile, and increasing CD8⁺ T-cell infiltration. This work establishes a reproducibly fabricated redox-active nanotherapeutic associated with mitochondrial stress that couples targeted chemotherapy with immune microenvironment remodeling for antitumor efficacy.
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8. Simultaneous broad-spectrum antibacterial and regenerative therapy for diabetic wounds using sonosensitive peptide composite hydrogel.
PMID:日期:2026-09-03Diabetic wound infections remain highly refractory to treatment due to persistent bacterial colonization, oxidative stress, dysregulated inflammation, vascular insufficiency, and impaired extracellular-matrix remodeling. Current therapeutic strategies remain limited by poor tissue penetration, inadequate infection control, and ineffective inflammatory-oxidative microenvironment modulation. Here, we engineered a sonosensitive antimicrobial peptide composite hydrogel, FFRK8@ZnO@fHAMA, by integrating human host-defense-peptide-derived FFRK8, microenvironment-responsive ZnO microspheres, and fish-collagen-modified hyaluronic acid methacrylate (fHAMA) into an injectable bioactive matrix. Upon low-intensity pulsed ultrasound (LIPUS) irradiation, this hydrogel acts as a multifunctional regenerative dressing that couple broad-spectrum bacterial eradication with oxidative-stress attenuation, macrophage repolarization, angiogenic activation and extracellular-matrix reconstruction. Distinct from conventional passive dressings or antibiotic-dependent therapies, FFRK8@ZnO@fHAMA enables non-invasive and spatiotemporally precise activation, sustained local therapeutic retention and coordinated immune-redox-metabolic microenvironment remodeling while maintaining favorable biosafety. This sonosensitive peptide hydrogel offers a powerful bioactive strategy for repairing infected diabetic wound and may inspire next-generation therapeutic modality for chronic non-healing tissue regeneration.
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9. Correction: ZnO colludes with C. acnes in healing delay and Scar hyperplasia by barrier destruction.
PMID:日期:2026-08-24该文献暂无摘要。