Journal of Nanobiotechnology最新文献

{"title":"SERSome-based metabolic profiling of aqueous humor for cataract subtyping with molecule-level interpretability.","authors":"Li Ning, Xinyuan Bi, Yepei Qin, Yinghong Ji, Jian Ye","doi":"10.1186/s12951-026-04789-1","DOIUrl":"10.1186/s12951-026-04789-1","url":null,"abstract":"<p><p>Cataract is among the leading cause of vision impairment worldwide and it is essential to uncover molecule-level characteristics of different cataract subtypes for personalized treatment. Compared to existing diagnostic techniques, surface-enhanced Raman spectroscopy (SERS) shows advantages in sensitive molecular fingerprinting, tractability and compactness, making it highly suitable for clinical adoption. To further address the current lack of SERS-based techniques for cataract subtyping, this work presented an integrated methodology for robust and interpretable metabolic profiling of aqueous humor. A two-step sample pretreatment protocol has been therein developed to efficiently extract metabolites while ensuring compatibility with subsequent SERS detection. SERSome strategy was employed to enable rapid and robust metabolic profiling. Molecule-level SERSome interpretation was achieved by matching its positive intra-correlation network with metabolites' SERS barcode. Multiple analytical methods including statistical comparison, interpretable machine learning, and association analysis have been leveraged, evidencing key metabolite biomarkers such as ergothioneine, hypoxanthine and uric acid associated with cataract subtyping and diabetic retinopathy. In a word, this study has not only established a systematic methodology for metabolic analysis of aqueous humor but also provided a usable tool for both fundamental research and clinical applications in different diseases with high rapidness, cost efficiency and scalability.</p>","PeriodicalId":16383,"journal":{"name":"Journal of Nanobiotechnology","volume":" ","pages":""},"PeriodicalIF":15.0,"publicationDate":"2026-07-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13631992/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148412084","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":"Effects and mechanism of carrier-free self-assembled nanoparticles of natural products in attenuating pulmonary edema.","authors":"Jin Yan, Kaixin Liu, Yuqi Yan, Zhenzhen Wang, Junfang Wang, Yingbo Wang, Yuanyuan Hou, Erwei Hao, Xiaotao Hou, Jie Gao, Gang Bai","doi":"10.1186/s12951-026-04777-5","DOIUrl":"10.1186/s12951-026-04777-5","url":null,"abstract":"<p><strong>Background: </strong>Pulmonary edema, a life-threatening condition in acute lung injury/acute respiratory distress syndrome (ALI/ARDS), is driven by dysregulated inflammation, barrier disruption, and alveolar fluid accumulation. Effective therapies that simultaneously target these multiple pathological processes with high lung specificity are urgently needed.</p><p><strong>Results: </strong>We engineered carrier-free, self-assembled nanoparticles from the natural products magnolol (Mag) and atractylenolide I (ATI) at an optimal 4:1 molar ratio. The Mag-ATI nanoparticles (MA NPs) exhibited an average hydrodynamic diameter of approximately 220.2 nm, excellent colloidal stability, and a pH-responsive release profile favorable for the acidic pulmonary microenvironment. The drug loading was 81.7 ± 0.356% for Mag and 18.2 ± 0.129% for ATI, encapsulation efficiency exceeded 97% for both. In a murine lipopolysaccharide (LPS)-induced ALI model, MA NPs potently ameliorated pulmonary edema, outperforming individual drugs or their physical mixture. Biodistribution studies confirmed the MA NPs' efficient lung accumulation, with a fluorescence intensity 3.6-5.9 times higher than in other organs, and specific targeting to alveolar epithelial cells. Mechanistically, Mag inhibited TRPV4-mediated Ca²⁺ influx, thereby suppressing the downstream cAMP/AQP5 axis to limit water permeability and restore alveolar fluid balance. Mag and ATI attenuated inflammatory signaling via the protein kinase B (AKT)/nuclear factor kappa B (NF‑κB) pathway. Furthermore, Mag and ATI preserved epithelial barrier integrity by stabilizing tight junction proteins. These multi-modal mechanisms were systematically validated both in vitro and in vivo. Importantly, MA NPs demonstrated a favorable safety profile with no significant systemic toxicity.</p><p><strong>Conclusion: </strong>This study presents a novel, carrier-free nanotherapeutic platform that integrates the efficacy-enhancing rationale of traditional herbal medicine with advanced nanoassembly. By enabling coordinated modulation of inflammation, barrier function, and fluid homeostasis, MA NPs offer a potent, targeted, and translational strategy for the treatment of ALI/ARDS.</p>","PeriodicalId":16383,"journal":{"name":"Journal of Nanobiotechnology","volume":" ","pages":""},"PeriodicalIF":15.0,"publicationDate":"2026-07-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13632447/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148412108","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":"Photoreceptor-targeted engineered exosomes encapsulating black phosphorus quantum dots for alleviating photoreceptor degeneration.","authors":"Jia Liang, Xiangqing Hei, Lu Chen, Zhenhua Zou, Yuke Ji, Lujia Feng, Wangting Li, Yijing Zhuang, Bingyu Bai, Renxue Liang, Yunyun Zou, Pan Xiao, Qiang Lin, Huiyan Zheng, Dong Fang, Wei Chi, Shaochong Zhang","doi":"10.1186/s12951-026-04763-x","DOIUrl":"10.1186/s12951-026-04763-x","url":null,"abstract":"<p><p>Photoreceptor degeneration is a major cause of irreversible visual impairment worldwide, most notably in retinitis pigmentosa (RP). Here, we developed a dual-targeted therapeutic nanoplatform by loading black phosphorus quantum dots (BPQDs) into human dental pulp mesenchymal stem cell-derived exosomes (hDPSC-Exos) and surface-modifying with cell-penetrating peptide transactivated transcription (TAT) and photoreceptor-specific peptide MH42, namely TAT/MH42-engineered black phosphorus quantum dot-loaded exosomes (M/T-BPQD@Exos). M/T-BPQD@Exos showed typical exosomal morphology and good uniformity. In vitro, M/T-BPQD@Exos effectively protected 661 W photoreceptor cells against N-methyl-N-nitrosourea (MNU) injury. In vivo, M/T-BPQD@Exos specifically accumulated in the outer nuclear layer (ONL) and significantly preserved retinal structure and visual function in MNU-induced photoreceptor degeneration rats. Biosafety assessment confirmed no obvious systemic toxicity and inflammation. Mechanistically, M/T-BPQD@Exos alleviated calcium overload, maintained mitochondrial integrity, and suppressed mitochondrial apoptosis by regulating Bcl-2, Bax, and cleaved caspase-3. This study provides a safe and precise strategy for photoreceptor protection in retinal degenerative diseases.</p>","PeriodicalId":16383,"journal":{"name":"Journal of Nanobiotechnology","volume":" ","pages":""},"PeriodicalIF":15.0,"publicationDate":"2026-07-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13459398/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148412111","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":"Targeting mitochondrial-ER homeostasis via autophagy inhibition with celastrol-based nanotherapy for triple-negative breast cancer.","authors":"Yuhao Ye, Xin Zhang, Qi Tong, Qiong Xie, Xuanming Gong, Siqi Du, Peiqin Gao, Qiushuang Li, Jigang Piao, Yang Xiong","doi":"10.1186/s12951-026-04769-5","DOIUrl":"10.1186/s12951-026-04769-5","url":null,"abstract":"<p><p>The functional crosstalk between mitochondria and the endoplasmic reticulum (ER) serves as a critical adaptive mechanism in cancer cells, wherein mitochondrial damage-induced ER stress can paradoxically activate protective mitophagy to restore cellular homeostasis and limit therapeutic efficacy. To subvert this self-repair cycle and amplify immunogenic cell death (ICD), we engineered a mitochondria-targeted biomimetic nanoplatform (Cel-Ca/CQ@OMM) for tumor-selective co-delivery of Celastrol (Cel) and Chloroquine (CQ). The nanosystem leverages homologous mitochondrial membrane functionalization to achieve precise subcellular localization. Celastrol coordinates with calcium ions to form a complex (Cel-Ca) that induces Ca²⁺ overload and reactive oxygen species (ROS) burst, thereby damaging mitochondria and concomitantly triggering lipophagy as a compensatory survival response. The ER, upon contact with damaged mitochondria, activates mitophagy to clear these organelles. By suppressing autophagic flux, CQ simultaneously abrogates both reparative mitophagy and adaptive lipophagy. The resulting cumulative accumulation of damaged mitochondria and lipid droplets perpetuates ER-mitochondria interaction and imposes metabolic burden on the ER, establishing a vicious cycle that progressively amplifies cellular stress through positive feedback regulation, thereby steering the cell toward apoptotic elimination. This dual-inhibition intervention disrupts mitochondrial-ER homeostasis, leading to exacerbated ER stress, enhanced damage-associated molecular pattern (DAMP) release, and robust CD8⁺ T cell-mediated antitumor immunity. This study highlights the amplification of ICD by synergistically blocking the key adaptive pathways of mitophagy and lipophagy, providing a promising approach for Triple-negative breast cancer (TNBC) treatment.</p>","PeriodicalId":16383,"journal":{"name":"Journal of Nanobiotechnology","volume":" ","pages":""},"PeriodicalIF":15.0,"publicationDate":"2026-07-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13435512/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148412087","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":"Advanced metal-phenolic networks for tissue regeneration: opportunities and challenges.","authors":"Meng Luo, Hongzhang Deng","doi":"10.1186/s12951-026-04470-7","DOIUrl":"10.1186/s12951-026-04470-7","url":null,"abstract":"<p><p>Owing to their commendable biocompatibility, unique physicochemical properties, and highly tunable structural characteristics, metal polyphenolic networks (MPNs) have emerged as a highly promising class of functional materials, exhibiting broad application prospects in the field of tissue regeneration. This study provides a comprehensive review of the effects of MPNs and their composites on cells and tissue regeneration. It meticulously highlights the mechanisms of action of MPNs and their primary synthesis methods. Furthermore, the properties of MPNs that facilitate tissue regeneration are discussed, along with their promotive effects on the repair of various tissues, including skin wounds, bone/cartilage, joints, the heart, nerves, and teeth. Finally, the challenges faced by MPNs are outlined, and future perspectives in this field are presented, aiming to provide new opportunities and pathways for the application of MPNs-based materials in tissue regeneration.</p>","PeriodicalId":16383,"journal":{"name":"Journal of Nanobiotechnology","volume":" ","pages":""},"PeriodicalIF":15.0,"publicationDate":"2026-07-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13628959/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148412134","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":"Lymph node metastasis-related circHELQ promotes progression and acts as a nanotherapeutic target in colorectal cancer.","authors":"Jingwen Peng, Wen Song, Mengzhen Lei, Min-Er Zhong, Ruijian Chen, Yuwei Liu, Haifeng Zhou, Yifan Liu, Zejian Lyu, Junyuan Deng, Jiatong Lin, Qi Zhang, Zihao Pan","doi":"10.1186/s12951-026-04693-8","DOIUrl":"10.1186/s12951-026-04693-8","url":null,"abstract":"<p><strong>Introduction: </strong>Studies have highlighted the important roles of circRNAs in various cancers. However, their specific functions in the lymph node metastasis (LNM) of colorectal cancer (CRC) remain largely unclear.</p><p><strong>Methods: </strong>The Arraystar human circRNA microarray was used to identify circular RNAs (circRNAs) associated with LNM in colorectal cancer (CRC). Quantitative real-time polymerase chain reaction (qRT-PCR) was performed to measure circHELQ expression in CRC cell lines and tissue specimens. A series of in vitro and in vivo functional assays were subsequently conducted to investigate the role of circHELQ in LNM and CRC progression. Additionally, fluorescence in situ hybridization, dual-luciferase reporter assays, RNA pull-down, and Western blot experiments were carried out to elucidate the underlying regulatory mechanisms of circHELQ in CRC.</p><p><strong>Results: </strong>Our results demonstrated that circHELQ expression was significantly upregulated in CRC and that its expression level was closely correlated with LNM. Gain- and loss-of-function experiments revealed that circHELQ promotes CRC progression and metastasis-including proliferation, migration, invasion, lymphatic vessel formation, and LNM-both in vitro and in vivo. Mechanistically, circHELQ acts as a competing endogenous RNA (ceRNA) that sponges miR-4793-3p, thereby alleviating its suppression of VEGFC. This circHELQ/miR-4793-3p/VEGFC axis drives LNM in CRC by upregulating VEGFC expression. Furthermore, we developed a cancer cell membrane-based siRNA delivery system (cMDS) targeting circHELQ, and these nanoparticles effectively suppressed CRC proliferation and LNM.</p><p><strong>Conclusions: </strong>CircHELQ drives CRC progression and LNM and is a candidate prognostic biomarker. Furthermore, its molecular function renders it a viable target for nanoparticle-based therapeutic strategies against CRC.</p>","PeriodicalId":16383,"journal":{"name":"Journal of Nanobiotechnology","volume":" ","pages":""},"PeriodicalIF":15.0,"publicationDate":"2026-07-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13629079/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148412072","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":"Glutathione-depleting self-immolative nanoparticles boost cuproptosis-driven metalloimmunotherapy for triple-negative breast cancer.","authors":"Yunhai Fu, Xiaoyu Wang, Yinqi Li, Xiaodong Yang, Ziying Yao, Jingwen Wang, Yaxin Zhang, Tianping Li, Yunke Zhu, Zhiyao He","doi":"10.1186/s12951-026-04668-9","DOIUrl":"10.1186/s12951-026-04668-9","url":null,"abstract":"<p><p>Despite advances in immunotherapy, triple-negative breast cancer (TNBC) remains a major therapeutic challenge owing to its marked aggressiveness, low immunogenicity, and limited responsiveness to immune checkpoint blockade (ICB). Herein, the esterase-responsive polymeric nanoparticles (EsCu@NPs) are developed. The polymer backbone covalently integrates an L-buthionine sulfoximine prodrug to inhibit glutathione biosynthesis, and the nanoparticle matrix encapsulates an elesclomol-copper complex to promote intratumoral copper accumulation. By concurrently depleting glutathione and perturbing copper homeostasis, EsCu@NPs elicit reinforced cuproptosis stress that is converted into immunogenic cell death. This process reprograms the suppressive tumor microenvironment, characterized by increased DC maturation, elevated CD8⁺ T-cell infiltration, and a reduction in regulatory T cells. These findings support enhanced cuproptosis-driven metalloimmunotherapy as a strategy for treating TNBC. Briefly, in neoadjuvant settings, preoperative EsCu@NPs reduce tumor burden, decrease minimal residual disease, curb postsurgical recurrence and spontaneous lung metastasis, translating into prolonged survival. Notably, combination with anti-PD-1 checkpoint blockade yields synergy, significantly enhancing the ICB responsiveness of TNBC and producing improved therapeutic efficacy. Overall, this study demonstrates that EsCu@NPs enable coordinated cuproptosis and immune reprogramming, expanding ICB efficacy and supporting a translatable neoadjuvant strategy in TNBC.</p>","PeriodicalId":16383,"journal":{"name":"Journal of Nanobiotechnology","volume":" ","pages":""},"PeriodicalIF":15.0,"publicationDate":"2026-07-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13625500/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148404147","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":"Single-cell transcriptomics-guided dynamic hydrogel delivery of artemisia argyi-derived EVs relieves ER stress and promotes diabetic wound regeneration.","authors":"Dazhuang Miao, Xiaopeng Suo, Xinqian Geng, Ying Yang, Gaoming Wang, Yang Zhou, Yunhe Jia, Shuofei Yang, Heping Li, Gaohua Li","doi":"10.1186/s12951-026-04759-7","DOIUrl":"10.1186/s12951-026-04759-7","url":null,"abstract":"<p><p>Diabetic wounds are characterized by persistent inflammation, impaired angiogenesis, and delayed tissue regeneration, yet effective strategies to regulate the pathological immune microenvironment remain limited. Here, integrated single-cell transcriptomics and multi-omics analyses revealed significant enrichment of endoplasmic reticulum stress (ERS)-related signaling in pro-inflammatory macrophages within diabetic wounds, suggesting a potential mechanism driving chronic inflammation. To target this process, we developed an injectable dynamic hydrogel (GPOK-2@EVs) incorporating Artemisia argyi-derived extracellular vesicles (EVs) for localized immunomodulatory therapy. The hydrogel was formed through dual dynamic crosslinking between phenylboronic acid-modified gelatin and oxidized konjac glucomannan, providing self-healing capability, injectability, tissue adhesion, and pH/ROS-responsive degradation for sustained EV release. In vitro experiments demonstrated that GPOK-2@EVs exhibited excellent biocompatibility and effectively reprogrammed macrophages toward an anti-inflammatory phenotype, accompanied by reduced inflammatory cytokine secretion, alleviated ERS activation, decreased ROS accumulation, and improved mitochondrial integrity. GPOK-2@EVs significantly enhanced endothelial angiogenic activities, including cytoskeletal remodeling, tube formation, and migration. In a diabetic mouse wound model, GPOK-2@EVs accelerated wound closure, promoted granulation tissue formation and collagen deposition, enhanced vascularization, and suppressed inflammatory and ERS responses. These findings demonstrate that EV-loaded dynamic hydrogels can modulate the inflammatory microenvironment and promote diabetic wound regeneration, providing a promising biomaterial strategy for chronic wound therapy.</p>","PeriodicalId":16383,"journal":{"name":"Journal of Nanobiotechnology","volume":" ","pages":""},"PeriodicalIF":15.0,"publicationDate":"2026-07-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13617955/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148391189","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":"Plant-derived extracellular vesicles as emerging cardioprotective agents for cardiovascular diseases.","authors":"Qian Li, Zhen Wang, Qianqian Huang, Nanbo Zheng, Bingtao Zhai, Dongyan Guo, Junbo Zou, Yajun Shi, Fei Luan","doi":"10.1186/s12951-026-04765-9","DOIUrl":"10.1186/s12951-026-04765-9","url":null,"abstract":"<p><p>Cardiovascular diseases (CVDs) remain a leading cause of global morbidity and mortality. Their complex and multifactorial pathogenesis, involving endothelial dysfunction, chronic inflammation, oxidative stress, metabolic dysregulation, and pathological remodeling, limits the long-term effectiveness of current therapeutic strategies and underscores the need for novel treatment approaches. Plant-derived extracellular vesicles (PDEVs) have recently emerged as promising cardioprotective agents because of their favorable biocompatibility, relatively low immunogenicity, abundant endogenous bioactive cargoes, and engineering flexibility. Owing to these properties, PDEVs possess dual characteristics as natural nanocarriers and bioactive therapeutic agents. Preclinical evidence from various in vitro and in vivo cardiovascular disease models indicates that PDEVs exert antioxidative, anti-inflammatory, immunomodulatory, and tissue-reparative effects, thereby attenuating myocardial injury, reducing oxidative stress, and promoting cardiomyocyte survival. Beyond their intrinsic therapeutic activities, PDEVs can also serve as multifunctional drug delivery vehicles for small-molecule drugs, nucleic acids, proteins, and natural bioactive compounds, improving cargo stability, bioavailability, and therapeutic performance. Recent advances in surface functionalization, membrane fusion, and biomimetic design have further enhanced their targeting capacity and functional controllability. This review focuses on the application of PDEVs in cardiovascular disease therapy, systematically summarizing their preparation, characterization, quality evaluation, and relative advantages and limitations compared with conventional nanocarriers. It further highlights their therapeutic effects in different cardiovascular disease models, drug delivery applications, engineering strategies, and the current progress and key challenges in clinical translation. Continued advances in this field may promote the translation of PDEVs from experimental research to clinical application and broaden their value in cardiovascular nanomedicine.</p>","PeriodicalId":16383,"journal":{"name":"Journal of Nanobiotechnology","volume":" ","pages":""},"PeriodicalIF":15.0,"publicationDate":"2026-07-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13617776/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148396908","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":"Peptide nanoarchitectonics of biomimetic nanozyme synergistically inhibits smooth muscle cell proliferation and promotes endothelial repair to reduce poststenting complications.","authors":"Xiyue Rong, Wenli Zhang, Sijin Chen, Tingting Xia, Yun Liu, Yi Wang, Lian Xu, Qianying Du, Ying Luo, Bo Liu, Jia Liu, Jie Xu, Yu Zhang, Dajing Guo","doi":"10.1186/s12951-026-04737-z","DOIUrl":"10.1186/s12951-026-04737-z","url":null,"abstract":"<p><p>Drug-eluting stents are effective for treating cardiovascular disease (CVD), but the procedure can cause mechanical damage to the endothelium, and the released antiproliferative agents delay reendothelialization and impair barrier function, ultimately leading to in-stent restenosis and disruption of vascular homeostasis. Current poststenting therapies, aimed at reducing proliferation and inflammation, often neglect endothelial cell (EC) repair and vascular homeostasis. To address this, we propose the use of a biomimetic nanozyme, HMPB-RAPA@PM&LXW7 (HRPL). Hollow mesoporous Prussian blue (HMPB) nanoparticles serve as carriers for the antiproliferative drug rapamycin (RAPA), which is further modified with a peptide nanoarchitectonics platelet membrane (PM&LXW7). This modification not only targets smooth muscle cells (SMCs) and ECs but also promotes EC repair to accelerate reendothelialization. In response to the acidic inflammatory microenvironment, HRPL releases RAPA to inhibit SMC proliferation and prevent restenosis. Additionally, the nanozyme scavenges reactive oxygen species (ROS), alleviates inflammation, and improves the vascular microenvironment. Both in vivo and in vitro experiments demonstrated that HRPL effectively accelerated reendothelialization, regulated SMC behavior, and reduced inflammation. In conclusion, this peptide nanoarchitectonics biomimetic nanozyme can promote endothelial repair, inhibit neointimal hyperplasia, modulate the inflammatory microenvironment, prevent restenosis, and restore vascular homeostasis, offering a promising approach to reduce complications following clinical stent implantation.</p>","PeriodicalId":16383,"journal":{"name":"Journal of Nanobiotechnology","volume":" ","pages":""},"PeriodicalIF":15.0,"publicationDate":"2026-07-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13617711/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148396900","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}