Huan Zhu, Zhaoyuan Zhang, Rong Jiang, Liangfu Xu, Xiangdi Yang, Jie Chen, Zhenning Wang, Xiao Xu, Zhigang Liu
{"title":"Correction: MXene-based nanosheet for enhanced glioma therapy via photonic hyperthermia to boost the abscopal effect of radioimmunotherapy.","authors":"Huan Zhu, Zhaoyuan Zhang, Rong Jiang, Liangfu Xu, Xiangdi Yang, Jie Chen, Zhenning Wang, Xiao Xu, Zhigang Liu","doi":"10.1186/s12951-026-04927-9","DOIUrl":"10.1186/s12951-026-04927-9","url":null,"abstract":"","PeriodicalId":16383,"journal":{"name":"Journal of Nanobiotechnology","volume":"24 1","pages":""},"PeriodicalIF":15.0,"publicationDate":"2026-08-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13501604/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148813344","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":"MHY@MO@PPP inhibits ferroptosis positive feedback and delays the acute kidney injury-to-chronic kidney disease transition by remodeling the Fe<sup>2+</sup>-mTORC1-GPX4 axis.","authors":"Chenhao Li, Chao Zhang, Chuanqi Zhang, Shiyu Duan, Jiali Zhang, Hongyue Wang","doi":"10.1186/s12951-026-04918-w","DOIUrl":"https://doi.org/10.1186/s12951-026-04918-w","url":null,"abstract":"<p><p>AKI-to-CKD progression is shaped by sustained tubular stress, ferroptosis-related iron imbalance, and oxidative injury. To target this process, we developed an MHY1485-loaded molybdenum oxide (MoOx) nanozyme coated with a pH-responsive phenylboronic acid-polyethylene glycol-phenylboronic acid (PBA-PEG-PBA) polymer (MHY@MO@PPP). We tested whether this platform could weaken the ferroptosis-associated injury loop and delay AKI-to-CKD transition through regulation of the Fe<sup>2+</sup>-mechanistic target of rapamycin complex 1 (mTORC1)-glutathione peroxidase 4 (GPX4) axis. Material properties were examined by dynamic light scattering (DLS), transmission electron microscopy (TEM), X-ray photoelectron spectroscopy (XPS), and liquid chromatography-tandem mass spectrometry (LC-MS/MS). Biological activity was assessed in erastin-induced ferroptotic human renal proximal tubular epithelial (HK-2) cells and in a C57BL/6 mouse unilateral ischemia-reperfusion injury (UIRI) model. MHY@MO@PPP showed stimulus-responsive MHY1485 release under simulated lesion-like conditions, lowered reactive oxygen species (ROS), lipid peroxidation, and free Fe<sup>2+</sup>, restored mitochondrial function, and improved cell survival. Mechanistic assays showed increased p-mTOR and GPX4 expression with reduced autophagy-related stress, supporting attenuation of the ferroptosis-related feedback state. Proteomic analysis and functional intervention experiments further implicated the Fe<sup>2+</sup>-mTORC1-GPX4 axis in the protective response. In vivo, MHY@MO@PPP improved renal function and reduced renal tissue injury and fibrosis. These findings support a nanozyme-based strategy that combines catalytic redox regulation with pathway modulation to mitigate AKI-to-CKD progression.</p>","PeriodicalId":16383,"journal":{"name":"Journal of Nanobiotechnology","volume":"24 1","pages":""},"PeriodicalIF":15.0,"publicationDate":"2026-08-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13625235/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149110615","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}
Chunjuan Jiang, Fengsheng Zhang, Simin He, Xuan Huang, Jiamin Zhu, Panli Li, Jindian Li, Xiangwei Wang, Shaoli Song
{"title":"AI-guided design of plectin-1-targeted <sup>68</sup>Ga-radiotracers reveals EP300-mediated membrane relocalization of plectin-1 in pancreatic ductal adenocarcinoma.","authors":"Chunjuan Jiang, Fengsheng Zhang, Simin He, Xuan Huang, Jiamin Zhu, Panli Li, Jindian Li, Xiangwei Wang, Shaoli Song","doi":"10.1186/s12951-026-04938-6","DOIUrl":"10.1186/s12951-026-04938-6","url":null,"abstract":"<p><strong>Background: </strong>Plectin-1 (PLEC) is a membrane-associated biomarker implicated in the progression of pancreatic ductal adenocarcinoma (PDAC) and is an attractive target for molecular imaging. However, peptide-based radiotracers targeting PLEC remain limited, and the mechanisms linking plectin-1 relocalization to aggressive biology have yet to be fully elucidated.</p><p><strong>Methods: </strong>In the present study, we performed stepwise in silico screening to identify membrane-associated metastatic drivers in PDAC. Then, we performed convolutional neural network-assisted docking to guide the design of <sup>68</sup>Ga-labeled NOTA-conjugated plectin-1-targeted monomeric (FZPN) and dimeric (FZPN-dimer) radiotracers. Radiochemical characterization, surface plasmon resonance, cellular uptake, blocking, pharmacokinetic, microPET/CT, biodistribution, and preliminary toxicity studies were then undertaken in PANC-1 models. Mechanistic studies assessed the subcellular localization of PLEC, its interaction with EP300, acetylation, and the functional role of lysine 1310 (K1310).</p><p><strong>Results: </strong>PLEC emerged as the top membrane-enriched, metastasis-linked, and prognostically adverse candidate for PDAC. Analysis demonstrated that the [<sup>68</sup>Ga]Ga-NOTA-FZPN-dimer exhibited high affinity for PLEC, favorable hydrophilicity and stability, and significantly higher cellular uptake and tumor accumulation than the monomeric tracer, with receptor-specific blockade in vitro and in vivo. In PANC-1 xenografts, tumor uptake of the dimer reached 3.8 ± 0.5%ID/g at 30 min after injection and remained higher than that of the monomer at all imaging time points. Mechanistically, PDAC tissues exhibited membrane-enriched PLEC; EP300 interacted with PLEC, acetylation was increased in PDAC cells, and the deacetylation-mimetic PLEC-K1310R mutant redirected plectin-1 away from the plasma membrane and reduced cell migration.</p><p><strong>Conclusions: </strong>Collectively, our findings show that [<sup>68</sup>Ga]Ga-NOTA-FZPN-dimer represents a promising PLEC-targeted PET radiotracer for molecular imaging in PDAC. EP300-mediated acetylation at K1310 appears to drive the membrane relocalization of PLEC and promote the migration of tumor cells, providing biological support for PLEC-targeted imaging and a rationale for further translational development.</p>","PeriodicalId":16383,"journal":{"name":"Journal of Nanobiotechnology","volume":"24 1","pages":""},"PeriodicalIF":15.0,"publicationDate":"2026-08-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13531995/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148864927","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}
Xinxin Liu, Luo Zhao, Liulu Wu, Yangyang Zhang, Yange Du, Ziqing Wang, Mengya Niu, Cuixia Zheng, Hongmin Liu, Lei Wang
{"title":"Probiotic-based sequential delivery system for gut-brain co-therapy against inflammatory bowel disease-associated anxiety/depression","authors":"Xinxin Liu, Luo Zhao, Liulu Wu, Yangyang Zhang, Yange Du, Ziqing Wang, Mengya Niu, Cuixia Zheng, Hongmin Liu, Lei Wang","doi":"10.1186/s12951-026-04850-z","DOIUrl":"https://doi.org/10.1186/s12951-026-04850-z","url":null,"abstract":"With the emergence of the gut-brain axis, inflammatory bowel disease (IBD) is no longer simply regarded as a localized intestinal disease but as a systemic disorder intimately associated with psychiatric comorbidities, including anxiety and depression. However, conventional therapeutic strategies predominantly target localized colonic inflammation, which often yields suboptimal outcomes. This highlights a critical need for gut-brain co-therapy to achieve comprehensive IBD management. Based on our observation that indole-3-acetic acid (IAA) possesses the potential to attenuate hippocampal neuroinflammation and subsequently modulate intestinal inflammation via the acetylcholine pathway, we engineered a gut-brain co-therapy delivery platform (CB-ASA/IAA/L). This system comprises Clostridium butyricum (CB) loaded with 5-aminosalicylic acid (5-ASA), encapsulated by a pH-responsive Eudragit L100-55 layer incorporating IAA. This microecological preparation is based on effective protection and delivery of CB, achieving the delivery of IAA to the brain and 5-ASA to the colon simultaneously. This sequential-release delivery system achieved intestinal barrier repair, promoted macrophage polarization toward the M2 phenotype, and restored Th17/Treg balance to recover intestinal homeostasis, while simultaneously alleviating anxiety- and depression-like behaviors in colitis mice. Importantly, the system demonstrated a robust ability to prevent inflammatory recurrence, a major clinical challenge in IBD treatment. This research offers a new avenue for the effective treatment of IBD-associated anxiety/depression by coordinating neuroimmune modulation with local intestinal repair. Schematic illustration of the synthesis, site-specific gastrointestinal delivery, and gut–brain axis-mediated therapeutic mechanisms of CB-ASA/IAA/L against inflammatory bowel disease and associated anxiety/depression.","PeriodicalId":16383,"journal":{"name":"Journal of Nanobiotechnology","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-08-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148861235","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}
Xuexue Liu, Chenxi Li, Wei Ge, Di Zhou, Yushuo Hao, Li Yi, Xiaolong Ma, Lihua Shao, Yuxiang Sun, Peipei Xu, Xiao Du, Siliang Wang
{"title":"FeDx-SF@βE assembly for AML treatment via GATA1/SLC40A1 pathway-mediated iron homeostasis disorder","authors":"Xuexue Liu, Chenxi Li, Wei Ge, Di Zhou, Yushuo Hao, Li Yi, Xiaolong Ma, Lihua Shao, Yuxiang Sun, Peipei Xu, Xiao Du, Siliang Wang","doi":"10.1186/s12951-026-04910-4","DOIUrl":"https://doi.org/10.1186/s12951-026-04910-4","url":null,"abstract":"Acute myeloid leukemia (AML) is an aggressive hematologic malignancy characterized by rapid progression, therapeutic resistance, and poor prognosis. Inducing ferroptosis in AML cells represents a promising therapeutic strategy. In this study, transcriptomic analyses first revealed that ferroptosis-associated transcriptional states were closely associated with prognosis and ex vivo drug-response heterogeneity in AML, providing a rationale for ferroptosis-oriented therapeutic design. Based on these findings, and further supported by a transcriptome-based target-scoring strategy, β-elemene (βE), a clinically used natural compound derived from traditional Chinese medicine, was selected as a candidate ferroptosis-related agent. We subsequently developed a nanodelivery system, designated FeDx-SF@βE, based on alcohol-induced silk fibroin (SF) folding to co-deliver ferric dextran (FeDx) and βE. The resulting nanoparticles exhibited a uniform particle size of 182.3 nm, favorable colloidal stability, and sustained drug release behavior. In vitro studies demonstrated efficient cellular uptake of FeDx-SF@βE by AML cells, leading to significantly inhibited cell viability. Pharmacological cell-death inhibitor rescue experiments showed that ferrostatin-1 produced the most pronounced protective effect, indicating that FeDx-SF@βE-induced AML cell death was predominantly ferroptosis-dependent. Mechanistically, βE-containing treatment suppressed the nuclear translocation of the transcription factor GATA1 and downregulated the iron efflux channel SLC40A1. GATA1/SLC40A1 gain- and loss-of-function analyses further demonstrated that activation of this axis attenuated FeDx-SF@βE-induced iron overload and ferroptotic injury, whereas suppression of this axis promoted intracellular iron retention, oxidative stress, lipid peroxidation, and mitochondrial damage. In combination with FeDx-derived iron supply, βE-mediated inhibition of the GATA1/SLC40A1 iron-export axis resulted in intracellular iron overload, glutathione depletion, ROS accumulation, extensive lipid peroxidation, and ferroptosis. Bulk transcriptomic and virtual-cell analyses further supported the involvement of the GATA1/SLC40A1 axis in ferroptosis-associated AML states and linked βE-related transcriptional programs to this regulatory mechanism. In a disseminated AML xenograft model, FeDx-SF@βE exhibited enhanced antileukemic efficacy and favorable biosafety. Collectively, this work provides a combined ferroptosis-oriented nanotherapeutic strategy for AML treatment and highlights the GATA1/SLC40A1 iron-homeostasis axis as a functionally relevant mechanism for ferroptosis-targeted nanomedicine design.","PeriodicalId":16383,"journal":{"name":"Journal of Nanobiotechnology","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-08-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148861234","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}