Journal of Nanobiotechnology最新文献

{"title":"Correction: Neutrophils mediated multistage nanoparticle delivery for prompting tumor photothermal therapy.","authors":"Bo Ye, Bao Zhao, Kun Wang, Yilong Guo, Qinguo Lu, Longpo Zheng, Ang Li, Jianou Qiao","doi":"10.1186/s12951-026-04717-3","DOIUrl":"10.1186/s12951-026-04717-3","url":null,"abstract":"","PeriodicalId":16383,"journal":{"name":"Journal of Nanobiotechnology","volume":"24 1","pages":""},"PeriodicalIF":15.0,"publicationDate":"2026-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13321441/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148361204","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction: Anti-EGFR ScFv functionalized exosomes delivering LPCAT1 specific siRNAsfor inhibition of lung cancer brain metastases.","authors":"Jun Jiang, Yuan Lu, Jie Chu, Xiao Zhang, Chao Xu, Shaojie Liu, Zhuo Wan, Jiawei Wang, Lu Zhang, Kui Liu, Zhenhua Liu, Angang Yang, Xinling Ren, Rui Zhang","doi":"10.1186/s12951-026-04714-6","DOIUrl":"10.1186/s12951-026-04714-6","url":null,"abstract":"","PeriodicalId":16383,"journal":{"name":"Journal of Nanobiotechnology","volume":"24 1","pages":""},"PeriodicalIF":15.0,"publicationDate":"2026-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13317423/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148361146","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cholesterol-depleted macrophage membrane-coated nano-rapamycin for targeted atherosclerosis therapy.","authors":"Ruru Zhang, Yan Liu, Zeyuan Cao, Zhe Yang, Nan Wen, Dongliang Hu, Kuan Lu, Keyang Xu, Xiao Xiao, Ning Wang, Mengdan Xu, Mengyao Wu, Yadan Shi, Xiuqi Hu, Ling Wen, Jianfeng Zeng, Wu Cai, Shenghong Ju","doi":"10.1186/s12951-026-04758-8","DOIUrl":"https://doi.org/10.1186/s12951-026-04758-8","url":null,"abstract":"<p><p>Atherosclerosis is the main pathological basis of cardiovascular disease and urgently requires more effective and targeted therapies. Here, we present a cholesterol-modulated macrophage membrane-mimetic nanoplatform for rapamycin delivery, in which β-cyclodextrin is employed to selectively deplete cholesterol from donor cell membranes. Cholesterol depletion significantly improves nanoparticle uptake by inflammatory macrophages, potentially through enhanced membrane fluidity and preserved key receptor-ligand interactions. In vitro, the cholesterol-depleted nanomedicines promote foam cell cholesterol efflux and suppress pro-inflammatory cytokine secretion, with therapeutic efficacy increasing as membrane cholesterol content decreases. In vivo, the resulting \"slimming\" membrane-coated nanoparticles exhibit enhanced immune evasion, prolonged systemic circulation, and improved plaque targeting, while maintaining excellent biosafety. In atherosclerotic mice, treatment with these nanoparticles reduces plaque area and lipid accumulation while increasing collagen content in a membrane cholesterol-dependent manner, indicating therapeutic effects and enhanced plaque stability. Notably, these benefits are achieved without altering systemic lipid levels, suggesting a primarily lesion-localized mechanism of action. Collectively, this study demonstrates that the \"slimming\" membrane-mimetic nanoplatform offers a promising approach for precise, inflammation-targeted therapy of atherosclerosis and may be extended to other chronic inflammatory vascular disorders.</p>","PeriodicalId":16383,"journal":{"name":"Journal of Nanobiotechnology","volume":" ","pages":""},"PeriodicalIF":15.0,"publicationDate":"2026-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148361162","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Publisher Correction: Exosome-mediated Piezo1 activation in 3D-printed titanium scaffolds promotes repair of femoral head osteonecrosis.","authors":"Yang Yu, Zhongyin Ji, Hongjun Xu, Mingyang Ma, Zhaojing Yin, Yiyang Du, Tao Zhang, Guiguan Wang, Feng Tian, Sen Liu, Jiajia Xue, Wenwei Qian","doi":"10.1186/s12951-026-04712-8","DOIUrl":"10.1186/s12951-026-04712-8","url":null,"abstract":"","PeriodicalId":16383,"journal":{"name":"Journal of Nanobiotechnology","volume":"24 1","pages":""},"PeriodicalIF":15.0,"publicationDate":"2026-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13321904/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148361152","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction: Targeting the oxidative microenvironment with a tannic acid-modified manganese dioxide nanozyme loaded with Honokiol nanoplatform to activate sirtuin 3-mediated deacetylation for alleviating cerebral ischemia-reperfusion injury.","authors":"Xin Yang, Yujing Cheng, Chengyuan Liu, Yuanju Chen, Ying Wang, Zhuang Li, Qiuxia Xiong, Chan Zhang","doi":"10.1186/s12951-026-04721-7","DOIUrl":"10.1186/s12951-026-04721-7","url":null,"abstract":"","PeriodicalId":16383,"journal":{"name":"Journal of Nanobiotechnology","volume":"24 1","pages":""},"PeriodicalIF":15.0,"publicationDate":"2026-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13322052/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148361215","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Publisher Correction: Prussian blue analogue-mineralized ginseng-derived vesicles promote PPARγ nuclear translocation to suppress tumor vasculogenic mimicry and reverse the immunosuppressive microenvironment.","authors":"Chaoqin Guo, Xiaoyan Zhang, Qiyi Liu, Xinxiu Shi, Xu Han, Qingqing Qiao, Yinan Li, Jingxia Han, Xiaoqing Chang, Yunlong Zhao, Huijuan Liu, Tao Sun","doi":"10.1186/s12951-026-04684-9","DOIUrl":"10.1186/s12951-026-04684-9","url":null,"abstract":"","PeriodicalId":16383,"journal":{"name":"Journal of Nanobiotechnology","volume":"24 1","pages":""},"PeriodicalIF":15.0,"publicationDate":"2026-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13321649/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148361149","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A zinc-coordinated cascade-responsive therapeutic nanoassembly for remodeling the pathological microenvironment and restoring mitochondrial homeostasis in spinal cord injury.","authors":"Chunyu Xiang, Xiaodong He, Fengshuo Guo, Haowen Luo, Liumin He, Wanguo Liu, Rui Gu","doi":"10.1186/s12951-026-04760-0","DOIUrl":"https://doi.org/10.1186/s12951-026-04760-0","url":null,"abstract":"<p><p>Secondary injury after spinal cord injury (SCI) is sustained by coupled oxidative stress and inflammation, which drives neuronal apoptosis and bioenergetic failure. Here, a cascade-responsive Zn²⁺-centered nanoassembly (Zn-PC/PA@Gel) is constructed through stepwise coordination among Zn²⁺, procyanidin (PC), and polyarginine (PA) to form a core-shell architecture with a Zn²⁺-procyanidin core (Zn-PC) and a Zn²⁺-polyarginine shell (Zn-PA). In a reactive oxygen species (ROS) rich injury microenvironment, oxidation of guanidino groups in the polyarginine shell enables in situ nitric oxide (NO) release and weakens Zn²⁺ coordination, triggering controlled shell disassembly for early modulation of local inflammation and tissue microenvironment. The subsequent release of PC and Zn²⁺ provides continuous antioxidant protection. Zn²⁺ further restores mitochondrial quality control by regulating the STAT3-FOXO3a-SOD2 axis, thus enhancing mitochondrial autophagy, enhancing endogenous antioxidant defense, and restoring mitochondrial homeostasis and energy metabolism. In a mouse spinal cord contusion model, Zn-PC/PA@Gel mitigated inflammation and oxidative stress, alleviated the burden of mitochondrial dysfunction, protected neurons, and promoted motor recovery, resulting in a Basso Mouse Scale (BMS) score of 7.0 on day 28. Overall, these results support Zn²⁺ coordinated cascade therapy nanoassembly, which combines microenvironmental regulation with mitochondrial homeostatic recovery to reduce secondary injury after SCI and promote locomotor improvement.</p>","PeriodicalId":16383,"journal":{"name":"Journal of Nanobiotechnology","volume":" ","pages":""},"PeriodicalIF":15.0,"publicationDate":"2026-06-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148352337","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Empagliflozin-pretreated mesenchymal stem cell-derived extracellular vesicles facilitate cardiac repair via AGGF1.","authors":"Qianwen Chen, Qingqing Gu, Jun Wei, Li Deng, Ye Deng, Jingyi Wang, Jianya Huang, Tingting Sun, Lu Pan, Wenjun Mao, Qingjie Wang, Ruxing Wang, Ling Sun","doi":"10.1186/s12951-026-04747-x","DOIUrl":"https://doi.org/10.1186/s12951-026-04747-x","url":null,"abstract":"<p><strong>Background: </strong>Current treatment modalities can only reap a limited efficacy in reversing myocardial damage and promoting functional recovery in patients with myocardial infarction. Therefore, there is an urgent need to explore new therapeutic approaches to enhance cardiac repair.</p><p><strong>Methods: </strong>MSCs were pretreated with empagliflozin to obtain EMPA-EVs, with non-pretreated MSC-EVs serving as controls. In vitro experiments were conducted to evaluate the effects of the two types of EVs on macrophage phenotypic transformation, cardiomyocyte apoptosis, and vascular endothelial cell lumen formation. In vivo experiments, a rat model of myocardial infarction was constructed, and EMPA-EVs, non-pretreated MSC-EVs, or phosphate-buffered saline were administered via myocardial injection. Post-treatment assessments included left ventricular ejection fraction, myocardial infarction area, and levels of pro-inflammatory cytokines in myocardial tissue. In addition, AGGF1 was depleted in EMPA-EVs to observe their anti-apoptotic, anti-inflammatory, and pro-angiogenic effects.</p><p><strong>Results: </strong>Compared with non-pretreated MSC-EVs, EMPA-EVs increased the proportion of macrophages transforming into anti-inflammatory phenotypes, decreased the rate of apoptotic cardiomyocytes, and promoted the formation of vascular endothelial cell lumen. Animal experiments showed that the left ventricular ejection fraction of rats in the EMPA-EVs group was higher than that in the control group, the myocardial infarction area was reduced, and the level of pro-inflammatory factors in myocardial tissue decreased. Moreover, AGGF1 expression was significantly upregulated in EMPA-EVs, and the anti-apoptotic, anti-inflammatory, and pro-angiogenic effects of EMPA-EVs were inhibited upon AGGF1 knockdown.</p><p><strong>Conclusion: </strong>EMPA-EVs can promote cardiac repair in myocardial infarction, and this therapeutic effect involves the upregulation of AGGF1 and may promise a cell-free therapeutic strategy.</p>","PeriodicalId":16383,"journal":{"name":"Journal of Nanobiotechnology","volume":" ","pages":""},"PeriodicalIF":15.0,"publicationDate":"2026-06-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148352347","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Aptamer-functionalized tetrahedral framework nucleic acid delivery of siBhlhe22 for repairing osteoporotic bone defects via dual modulation of PI3K-Akt signaling and purine metabolism.","authors":"Qiaonan Ye, Long Bai, Yue Gao, Shiyi Zeng, Zhiyuan Zhang, Yong Li, Qianke Tao, Maorui Zhang, Yunfeng Lin, Jingang Xiao","doi":"10.1186/s12951-026-04706-6","DOIUrl":"https://doi.org/10.1186/s12951-026-04706-6","url":null,"abstract":"<p><p>Osteoporosis is characterized by an imbalance between bone formation and resorption, and the dysregulated differentiation of bone marrow mesenchymal stem cells (BMSCs) plays a central role. Our previous study identified Bhlhe22 as a key negative regulator of osteogenic differentiation; here, we further validate its role in osteoporotic BMSCs (OP-BMSCs) and investigate its therapeutic potential. Knocking down Bhlhe22 enhanced osteogenesis by upregulating key osteogenic markers (RUNX2, ALP, OPN) and suppressing the PI3K-Akt signaling pathway. To enable targeted delivery of siBhlhe22, we designed an aptamer-functionalized tetrahedral framework nucleic acid-based nanocarrier (Apt19S-tFNA-siBhlhe22, ATS). The ATS system exhibited well-defined nanostructure, excellent biocompatibility, and high cellular uptake efficiency in OP-BMSCs. In vitro, ATS-mediated Bhlhe22 knockdown significantly promoted osteogenic differentiation and matrix mineralization. This effect depended on the inhibition of PI3K-Akt signaling, as demonstrated by rescue experiments using the agonist Recilisib. Non-targeted metabolomics revealed that osteoporosis was associated with disruption of nucleotide and purine metabolism, which was effectively reversed by ATS treatment. Functional studies confirmed that intact purine metabolism, which was essential for ATP production and redox balance, was required for the pro-osteogenic effect of ATS. In an osteoporotic rat bone defect model, ATS delivered via GelMA hydrogel promoted bone regeneration. This was accompanied by in vivo suppression of PI3K-Akt signaling and upregulation of OCN and OPN. Our findings establish a novel gene therapy strategy that targets Bhlhe22 to simultaneously modulate pro-osteogenic signaling and metabolic reprogramming, offering a promising anabolic approach for osteoporosis treatment.</p>","PeriodicalId":16383,"journal":{"name":"Journal of Nanobiotechnology","volume":" ","pages":""},"PeriodicalIF":15.0,"publicationDate":"2026-06-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148345536","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dual-single-atom nanozyme with stage-adaptive catalytic regulation for infected diabetic wound healing.","authors":"Jian Zhang, Jihai Xu, Chengchun Shen, Peilong Jiang, Heyang Sun, Jian Ruan, Yaopeng Huang, Xin Hong, Shengbing Yang, Hong Chen, Guoping Shi, Xin Wang","doi":"10.1186/s12951-026-04728-0","DOIUrl":"https://doi.org/10.1186/s12951-026-04728-0","url":null,"abstract":"<p><p>Infected diabetic wounds remain difficult to treat because persistent bacterial reservoirs coexist with a failure to transition from antibacterial defense to regenerative repair. Here, we report a dual-single-atom nanozyme (FeCo-CN) in which atomically dispersed Fe and Co centers are anchored within a nitrogen-coordinated carbon framework, enabling stage-adaptive regulation of the wound microenvironment. During the early infection phase, FeCo-CN exhibits photothermal-enhanced peroxidase-like activity that efficiently reduces extracellular bacteria and promotes macrophage-mediated intracellular bacterial clearance. As the bacterial burden decreases, the material shows superoxide dismutase- and catalase-like activities that alleviate oxidative stress, preserve mitochondrial function, and favor the shift toward reparative immune responses. These coordinated effects support angiogenesis and tissue regeneration. Overall, this work highlights a dual-single-atom nanozyme strategy that integrates infection control with immune transition and tissue repair in infected diabetic wounds.</p>","PeriodicalId":16383,"journal":{"name":"Journal of Nanobiotechnology","volume":" ","pages":""},"PeriodicalIF":15.0,"publicationDate":"2026-06-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148345553","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}