Journal of Nanobiotechnology最新文献_第5页

Revolutionizing brain‒computer interfaces: overcoming biocompatibility challenges in implantable neural interfaces. 革新脑机接口：克服植入式神经接口的生物相容性挑战。

IF 10.6 1区生物学

Journal of Nanobiotechnology Pub Date : 2025-07-10 DOI: 10.1186/s12951-025-03573-x

Weihang Gao, Zineng Yan, Hong Zhou, Yi Xie, Honglin Wang, Jiaming Yang, Jingbo Yu, Changmao Ni, Pengran Liu, Mao Xie, Li Huang, Zhewei Ye

{"title":"Revolutionizing brain‒computer interfaces: overcoming biocompatibility challenges in implantable neural interfaces.","authors":"Weihang Gao, Zineng Yan, Hong Zhou, Yi Xie, Honglin Wang, Jiaming Yang, Jingbo Yu, Changmao Ni, Pengran Liu, Mao Xie, Li Huang, Zhewei Ye","doi":"10.1186/s12951-025-03573-x","DOIUrl":"10.1186/s12951-025-03573-x","url":null,"abstract":"Brain‒computer interfaces (BCIs) exhibit significant potential for various applications, including neurofeedback training, neurological injury management, and language, sensory and motor rehabilitation. Neural interfacing electrodes are positioned between external electronic devices and the nervous system to capture complex neuronal activity data and promote the repair of damaged neural tissues. Implantable neural electrodes can record and modulate neural activities with both high spatial and high temporal resolution, offering a wide window for neuroscience research. Despite significant advancements over the years, conventional neural electrode interfaces remain insufficient for fully achieving these objectives, particularly in the context of long-term implantation. The primary limitation stems from the poor biocompatibility and mechanical mismatch between the interfacing electrodes and neural tissues, which induce a local immune response and scar tissue formation, thus decreasing the performance and useful lifespan. Therefore, neural interfaces should ideally exhibit appropriate stiffness and minimal foreign body reactions to mitigate neuroinflammation and enhance recording quality. This review provides an exhaustive analysis of the current understanding of the critical failure modes that may impact the performance of implantable neural electrodes. Additionally, this study provides a comprehensive overview of the current research on coating materials and design strategies for implanted neural interfaces and discusses the primary challenges currently facing long-term implantation of neural electrodes. Finally, we present our perspective and propose possible future research directions to improve implantable neural interfaces for BCIs.","PeriodicalId":16383,"journal":{"name":"Journal of Nanobiotechnology","volume":"23 1","pages":"498"},"PeriodicalIF":10.6,"publicationDate":"2025-07-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12243264/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144608608","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}

引用次数: 0

Differences in macrophage pyroptosis and polarization induced by nano-/micro-calcium oxalate crystals. 纳米/微草酸钙晶体诱导巨噬细胞焦亡和极化的差异。

IF 10.6 1区生物学

Journal of Nanobiotechnology Pub Date : 2025-07-10 DOI: 10.1186/s12951-025-03549-x

Xin-Yi Tong, Wei-Jian Nong, Run-Min Tan, Jian-Ming Ouyang

{"title":"Differences in macrophage pyroptosis and polarization induced by nano-/micro-calcium oxalate crystals.","authors":"Xin-Yi Tong, Wei-Jian Nong, Run-Min Tan, Jian-Ming Ouyang","doi":"10.1186/s12951-025-03549-x","DOIUrl":"10.1186/s12951-025-03549-x","url":null,"abstract":"Objective: This study aimed to compare the differences in pyroptosis and polarization of macrophages induced by different sizes of calcium oxalate monohydrate (COM) crystals and discuss the mechanism of kidney stone formation.Methods: COM crystals with sizes of about 100 nm, 500 nm, 2.5 μm, and 10 μm were synthesized and characterized. THP-1 cells were induced to differentiate into macrophage-like cells. The damage of COM crystals to Mφs was evaluated by CCK-8 assay. The activation of the pyroptosis signaling pathway, cell morphology, and proportion of pyroptosis cells in Mφs induced by COM crystals were detected. Finally, the proportion of M1/M2 polarization was qualitatively and quantitatively assessed.Results: COM-100 nm, COM-500 nm, COM-2.5 μm, and COM-10 μm all significantly induced the pyroptosis and polarization of Mφs. Among them, at the same cell viability, COM-10 μm induced the highest pyroptosis rate. The expression of NLRP3 and GSDMD-N induced by COM-10 μm increased by 81.43 ± 11.45% and 112.00 ± 9.87%, respectively, and the rate of caspase-1/PI double-positive pyroptosis cells was 22.2%. Meanwhile, COM-10 μm induced the highest proportion of M1 polarization (M1/M2 ratio was 209.90% ± 2.54%).Conclusion: COM-10 μm significantly activates the classical caspase-1-mediated pyroptosis pathway and promotes M1 polarization in Mφs. Therefore, at the same cell viability, large-sized micro-COM is more capable of inducing inflammation than nano-COM.","PeriodicalId":16383,"journal":{"name":"Journal of Nanobiotechnology","volume":"23 1","pages":"499"},"PeriodicalIF":10.6,"publicationDate":"2025-07-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12243305/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144608607","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}

引用次数: 0

A GSH-consuming polymeric nanoparticles drives ferroptosis amplification and combines chemotherapy to amplify breast cancer treatment. 一种消耗谷胱甘肽的聚合纳米颗粒驱动铁下垂扩增，并结合化疗来扩大乳腺癌治疗。

IF 10.6 1区生物学

Journal of Nanobiotechnology Pub Date : 2025-07-09 DOI: 10.1186/s12951-025-03569-7

Mingliang Pei, Xin Guan, Xiaodong Hou, Zhiyuan Niu, Qi Lyu, Kai Wang, Shanshan Wang, Jingkai Zhang, Yun Ke, Shuting Zhuang, Jie Chen, Huixiong Xu, Fan Yang

{"title":"A GSH-consuming polymeric nanoparticles drives ferroptosis amplification and combines chemotherapy to amplify breast cancer treatment.","authors":"Mingliang Pei, Xin Guan, Xiaodong Hou, Zhiyuan Niu, Qi Lyu, Kai Wang, Shanshan Wang, Jingkai Zhang, Yun Ke, Shuting Zhuang, Jie Chen, Huixiong Xu, Fan Yang","doi":"10.1186/s12951-025-03569-7","DOIUrl":"10.1186/s12951-025-03569-7","url":null,"abstract":"Currently, given variations in the abnormal tumor microenvironment (TME), significant progress has been made in the treatment of breast cancer (BC) based on TME-responsive nanosystems-mediated ferroptosis. Due to inherent deficiencies such as the limited efficacy of Fe-induced catalysis, the lack of endogenous hydrogen peroxide (H2O2), and the overexpression of glutathione (GSH) in tumor cells, the treatment of ferroptosis is restricted. Here, this document highlighted polymeric nanoparticles with GSH resection (ssP-tHB@Fe/DOX), demonstrating significant improvements in TME responses, biocompatibility, and anti-tumor effects. Our study offers a platform for combined BC amplification therapy involving ferroptosis and DOX-induced chemotherapy, and it highlights the use of 3,4,5-trihydroxybenzaldehyde (tHB) in a Fe(III)-Fe(II) cyclic reaction to deplete GSH and enhance ferroptosis. Notably, ssP-tHB@Fe/DOX could effectively disrupt mitochondrial structure and reduce membrane potential in tumor cells, leading to decreased ATP production, depletion of GSH via multi-channel approach, inhibition of GPX4 expression, and accumulation of lipid peroxidation, thereby inducing ferroptosis enhancement to achieve BC therapy. Meanwhile, the release of the anticancer drug DOX has dual effects: it interferes with NADPH to enhance the Fe-mediated Fenton reaction and induces apoptosis in tumor cells. Moreover, RNA sequencing (RNA-seq) analysis robustly supported the anti-tumor mechanism of ssP-tHB@Fe/DOX, confirming involvement in the amino acid metabolism ferroptosis signaling pathway and the p53 signaling pathway, etc. Therefore, in this study, we thoroughly introduced the design of intelligent nanosystems, proposed methods to enhance DOX-induced apoptosis and ferroptosis, offering a novel approach for cancer treatment.","PeriodicalId":16383,"journal":{"name":"Journal of Nanobiotechnology","volume":"23 1","pages":"497"},"PeriodicalIF":10.6,"publicationDate":"2025-07-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12239343/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144600727","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}

引用次数: 0

Mitochondrial homeostasis restoring peptide-drug conjugates with ROS-responsive NO releasing ability for targeted therapy of myocardial infarction. 恢复线粒体稳态的肽-药物偶联物与ros反应性NO释放能力用于心肌梗死的靶向治疗。

IF 10.6 1区生物学

Journal of Nanobiotechnology Pub Date : 2025-07-08 DOI: 10.1186/s12951-025-03578-6

Zhaoyang Lu, Quanyou Chai, Wenbin Dai, Bo Yu, Qingbo Lv, Fuyu Qiu, Jing Gao, Juhong Zhang, Xiaohua Shen, Shengyu Chen, Zhida Shen, Min Shang, Wenbin Zhang, Guosheng Fu, Qiao Jin, Yanbo Zhao, Fan Jia

{"title":"Mitochondrial homeostasis restoring peptide-drug conjugates with ROS-responsive NO releasing ability for targeted therapy of myocardial infarction.","authors":"Zhaoyang Lu, Quanyou Chai, Wenbin Dai, Bo Yu, Qingbo Lv, Fuyu Qiu, Jing Gao, Juhong Zhang, Xiaohua Shen, Shengyu Chen, Zhida Shen, Min Shang, Wenbin Zhang, Guosheng Fu, Qiao Jin, Yanbo Zhao, Fan Jia","doi":"10.1186/s12951-025-03578-6","DOIUrl":"10.1186/s12951-025-03578-6","url":null,"abstract":"Myocardial infarction (MI) is the leading cause of death worldwide. Exogenous delivery of nitric oxide (NO) shows great potential in MI treatment. However, the burst generation of reactive oxygen species (ROS) in ischemic microenvironment of MI oxidize NO to harmful peroxynitrite (ONOO-). It renders secondary damage to cardiomyocyte, causing the failure of NO based therapies. Herein, we proposed an ROS responsive peptide-drug conjugates (PDCs) to overcome the dilemma of NO based therapy. The conjugated cardiac injury targeting peptide (CTP) in the PDC (named CTP-PBA-ISN) promoted selective accumulation of drugs in MI sites. Besides, controlled release of NO prodrug isosorbide mononitrate (ISN) was achieved by pathological ROS triggered hydrolysis of boronate ester. Meanwhile the antioxidant byproduct 4-hydroxybenzyl alcohol further scavenges the overwhelming ROS, reducing the production of RNS and improving the bioavailability of NO. The CTP-PBA-ISN efficiently inhibited myocardial apoptosis, improved myocardial function, and ameliorated adverse cardiac remodeling post-MI in mice by relief of oxidative stress, promotion of angiogenesis and restoration of mitochondrial homeostasis and function. These findings prove that the synergic ROS regulation is essential in maximizing therapeutic effects of NO. Our CTP-PBA-ISN may serve as a valuable inspiration for development of other treatments of myocardial infarction and other ischemic diseases.","PeriodicalId":16383,"journal":{"name":"Journal of Nanobiotechnology","volume":"23 1","pages":"496"},"PeriodicalIF":10.6,"publicationDate":"2025-07-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12236005/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144591468","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}

引用次数: 0

Recent advances of engineering cell membranes for nanomedicine delivery across the blood-brain barrier. 纳米药物通过血脑屏障的工程细胞膜研究进展。

IF 10.6 1区生物学

Journal of Nanobiotechnology Pub Date : 2025-07-08 DOI: 10.1186/s12951-025-03572-y

Shengnan Yuan, Dehong Hu, Duyang Gao, Christopher J Butch, Yiqing Wang, Hairong Zheng, Zonghai Sheng

{"title":"Recent advances of engineering cell membranes for nanomedicine delivery across the blood-brain barrier.","authors":"Shengnan Yuan, Dehong Hu, Duyang Gao, Christopher J Butch, Yiqing Wang, Hairong Zheng, Zonghai Sheng","doi":"10.1186/s12951-025-03572-y","DOIUrl":"10.1186/s12951-025-03572-y","url":null,"abstract":"The blood-brain barrier (BBB) poses a major challenge to the effective delivery of therapeutic agents for the treatment of central nervous system (CNS) disorders. The integration of cell membrane engineering with nanotechnology has recently enabled the development of membrane-engineered nanoparticles (CNPs). These nanocarriers exhibit enhanced BBB penetration and improved CNS targeting. This review systematically summarizes the latest advances in the development and application of CNPs, emphasizing how different cellular sources-such as erythrocytes, platelets, tumor cells, and leukocytes-impact delivery efficiency and therapeutic outcomes. We also examine the molecular mechanisms underlying nanoparticle-BBB interactions and highlight the importance of biosafety evaluations. Moreover, critical barriers to clinical translation, including large-scale manufacturing challenges, batch-to-batch variability, and regulatory complexities, are discussed. Finally, we explore emerging strategies-particularly the integration of artificial intelligence (AI)-that hold potential for overcoming existing clinical gaps, enabling the rational design and optimized development of CNP-based therapeutics for CNS disorders. By integrating mechanistic insights with translational perspectives, this review provides a clear conceptual and technological foundation for the development of next-generation CNS-targeted nanotherapeutics.","PeriodicalId":16383,"journal":{"name":"Journal of Nanobiotechnology","volume":"23 1","pages":"493"},"PeriodicalIF":10.6,"publicationDate":"2025-07-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12235962/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144584157","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}

引用次数: 0

Synergizing sono-piezo with exosome suppression using doping-engineered hydroxyapatite for potentiated tumor treatment through immunoactivation. 利用掺杂工程羟基磷灰石协同声纳压电和外泌体抑制，通过免疫激活增强肿瘤治疗。

IF 10.6 1区生物学

Journal of Nanobiotechnology Pub Date : 2025-07-08 DOI: 10.1186/s12951-025-03564-y

Xinran Qu, Qin Fan, Yingying Liu, Jinqiao Zhang, Boyu Yuan, Xianzhou Cai, Luli Ji, Rulin Zhuang, Ziliang Dong

{"title":"Synergizing sono-piezo with exosome suppression using doping-engineered hydroxyapatite for potentiated tumor treatment through immunoactivation.","authors":"Xinran Qu, Qin Fan, Yingying Liu, Jinqiao Zhang, Boyu Yuan, Xianzhou Cai, Luli Ji, Rulin Zhuang, Ziliang Dong","doi":"10.1186/s12951-025-03564-y","DOIUrl":"10.1186/s12951-025-03564-y","url":null,"abstract":"Piezoelectric nanomaterials that generate reactive oxygen species (ROS) through piezoelectric polarization under mechanical stimulation have emerged as a promising cancer therapy platform. However, their potential is limited by poor piezoresponse, low catalytic efficiency, and the exacerbation of immunosuppression due to ROS-induced release of tumor-derived exosomes. In this study, we employed a doping-engineered strategy by incorporating manganese ions (Mn2⁺) into hydroxyapatite (HAP) to enhance its piezocatalytic performance, while combining exosome inhibition to achieve a synergistic improvement in tumor therapy. Mn2⁺-doped HAP was synthesized via a one-pot hydrothermal method and subsequently modified with a ROS-cleavable lipid, DSPE-TK-mPEG. During the modification process, the exosome inhibitor GW4869 was loaded, resulting in the formation of GW4869-loaded Mn2⁺-HAP-Lipid nanocomposites (abbreviated as GMHL). The introduction of Mn2+ significantly reduced the bandgap of HAP, thereby enhancing its piezoelectric catalytic activity to generate ROS under ultrasound (US) stimulation, which triggered the cleavage of ketone-thiol bond in DSPE-TK-mPEG and led to the efficient release of GW4869. In multiple tumor models, GMHL effectively retard tumor growth and inhibited the production of tumor-derived exosomal PD-L1 upon US stimulation, thereby triggering an anticancer immune response through modulation of the immunosuppressive tumor microenvironment.","PeriodicalId":16383,"journal":{"name":"Journal of Nanobiotechnology","volume":"23 1","pages":"495"},"PeriodicalIF":10.6,"publicationDate":"2025-07-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12235841/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144584168","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}

引用次数: 0

Quercetin nanoformulation-embedded hydrogel inhibits osteopontin mediated ferroptosis for intervertebral disc degeneration alleviation. 槲皮素纳米配方嵌入水凝胶抑制骨桥蛋白介导的铁下垂减轻椎间盘退变。

IF 10.6 1区生物学

Journal of Nanobiotechnology Pub Date : 2025-07-08 DOI: 10.1186/s12951-025-03574-w

Jitian Li, Lemeng Ren, Lei Wan, Man Liu, Mingyu Zhao, Yazhou Lin, Jiancheng Zheng, Yun Tang, Yage Luo, Yan Ma, Lei Wang, Peng Cao, Zhe Chen, Wenjie Ren, Fei Wang

{"title":"Quercetin nanoformulation-embedded hydrogel inhibits osteopontin mediated ferroptosis for intervertebral disc degeneration alleviation.","authors":"Jitian Li, Lemeng Ren, Lei Wan, Man Liu, Mingyu Zhao, Yazhou Lin, Jiancheng Zheng, Yun Tang, Yage Luo, Yan Ma, Lei Wang, Peng Cao, Zhe Chen, Wenjie Ren, Fei Wang","doi":"10.1186/s12951-025-03574-w","DOIUrl":"10.1186/s12951-025-03574-w","url":null,"abstract":"Reactive oxygen species (ROS) play a pivotal role in multiple events during the progression of intervertebral disc degeneration (IDD). Hence, the precision treatment targets associated with ROS should be further explored to promote developing effective therapeutic strategies. In this study, by analyzing specimens from patients and RNA sequencing of ROS-induced human primary nucleus pulposus cells (NPCs), osteopontin (OPN) and ferroptosis were identified as critical molecular entities and cellular pathways implicated in ROS-mediated IDD. Subsequent animal models and cellular assays determined that ROS induced upregulation of OPN, which in turn triggered ferroptosis in NPCs and intervertebral discs, consequently leading to IDD. Building upon these findings, a comprehensive screening of molecular drug database revealed that quercetin, an antioxidant molecule compound, possesses the capacity to couple OPN, thereby mitigating OPN-induced ferroptosis and IDD. In addition, the compound of quercetin for targeting OPN was encapsulated in phenylboric acid modified dendrimer (G3-PBA) nanoparticles to improve its solubility, and then embedded in a ROS-degradable and injectable hydrogel, thereby achieving on-demand release of quercetin with the progression of IDD. Collectively, this study not only identified a novel therapeutic target, but also engineered an effective therapeutic strategy intended for the autonomous management of IDD.","PeriodicalId":16383,"journal":{"name":"Journal of Nanobiotechnology","volume":"23 1","pages":"492"},"PeriodicalIF":10.6,"publicationDate":"2025-07-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12235785/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144584156","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}

引用次数: 0

PIEZO2 is the underlying mediator for precise magnetic stimulation of PVN to improve autism-like behavior in mice. PIEZO2是PVN精确磁刺激改善小鼠自闭症样行为的潜在介质。

IF 10.6 1区生物学

Journal of Nanobiotechnology Pub Date : 2025-07-08 DOI: 10.1186/s12951-025-03557-x

Sha Liu, Xuan Liu, Yefan Duan, Li Huang, Tong Ye, Ning Gu, Tao Tan, Zhijun Zhang, Jianfei Sun

{"title":"PIEZO2 is the underlying mediator for precise magnetic stimulation of PVN to improve autism-like behavior in mice.","authors":"Sha Liu, Xuan Liu, Yefan Duan, Li Huang, Tong Ye, Ning Gu, Tao Tan, Zhijun Zhang, Jianfei Sun","doi":"10.1186/s12951-025-03557-x","DOIUrl":"10.1186/s12951-025-03557-x","url":null,"abstract":"The precision magnetic stimulation system (pMSS), mediated by superparamagnetic iron oxide nanoparticles (SPIONs), can modulate endogenous oxytocin secretion by targeting the paraventricular nucleus (PVN) and improve autistic-like behavior in mice. In this study, the underlying mechanisms of this system were explored. Our findings demonstrate that pMSS bi-directionally regulates oxytocin secretion, inhibiting secretion at a low frequency (1 Hz) and promoting secretion at a high frequency (10 Hz). Transcriptome screening and replicate validation reveal that 10 Hz-pMSS promotes the expression of mechanosensitive Piezo2 channels on oxytocinergic neurons, increasing neuronal calcium influx and activating oxytocin and PI3K-Akt signaling pathways. Specific knockdown of Piezo2 in PVN blocks the effect of 10 Hz-pMSS, improving autistic-like behavior in mice. Mechanistically, valproic acid-induced autism model mice exhibit low oxytocin secretion and inhibition of neurite growth, and magnetomechanical stimulation by 10 Hz-pMSS can reverse these differences. Thus, 10 Hz-pMSS targeting the PVN rapidly reduces autistic-like behaviors in mice mediated by activation of Piezo2 in the PVN, increased neuronal calcium influx, and alterations in oxytocin secretion and neurite growth.","PeriodicalId":16383,"journal":{"name":"Journal of Nanobiotechnology","volume":"23 1","pages":"494"},"PeriodicalIF":10.6,"publicationDate":"2025-07-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12235948/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144584155","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}

引用次数: 0

Self-assembled transdermal nanogels control scar formation by inhibiting fibroblast proliferation and fibrosis with glycolysis regulation via the PI3K/Akt/mTOR pathway. 自组装透皮纳米凝胶通过糖酵解调控PI3K/Akt/mTOR途径抑制成纤维细胞增殖和纤维化，从而控制瘢痕形成。

IF 10.6 1区生物学

Journal of Nanobiotechnology Pub Date : 2025-07-07 DOI: 10.1186/s12951-025-03562-0

Xinxian Meng, Zhixi Yu, Shiqi Wu, Wanyu Xu, Yuzhen Tang, Zixuan Chen, Yixin Zhang, Yunsheng Chen, Zheng Zhang

{"title":"Self-assembled transdermal nanogels control scar formation by inhibiting fibroblast proliferation and fibrosis with glycolysis regulation via the PI3K/Akt/mTOR pathway.","authors":"Xinxian Meng, Zhixi Yu, Shiqi Wu, Wanyu Xu, Yuzhen Tang, Zixuan Chen, Yixin Zhang, Yunsheng Chen, Zheng Zhang","doi":"10.1186/s12951-025-03562-0","DOIUrl":"10.1186/s12951-025-03562-0","url":null,"abstract":"Hypertrophic scar (HS) is one of the most common challenges in the field of plastic and reconstructive surgery. HS formation is associated with the abnormal activation of fibroblasts. These fibroblasts exhibit excessive proliferative and fibrotic behavior, which can be induced by glycolysis dysregulation. Herein, self-assembled nanogels prepared by modifying IR808 with hyaluronic acid (termed HA-IR808) are introduced as selective glycolytic inhibitors to control HS formation through transdermal delivery to HS fibroblasts (HFs). HA-IR808 preferentially targets activated HFs and has a structure suitable for transdermal delivery. In vitro, HA-IR808 exhibits a glycolysis inhibition effect and regulates the fibrotic behavior and proliferation of HFs through energy depletion and macromolecule synthesis. In vivo, HA-IR808 penetrates the dermal layer, regulates glycolysis, and controls HS formation. Mechanistically, HA-IR808 regulates glycolysis by silencing the phosphatidylinositol 3-kinase (PI3K)/Akt/mammalian target of the rapamycin (mTOR) signaling pathway. In conclusion, this research elucidates a strategy for controlling HS formation via glycolysis regulation using self-assembled HA-IR808 nanogels to inhibit HF activation.","PeriodicalId":16383,"journal":{"name":"Journal of Nanobiotechnology","volume":"23 1","pages":"491"},"PeriodicalIF":10.6,"publicationDate":"2025-07-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12232762/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144584167","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}

引用次数: 0

Macrophage-mimetic liposomes co-delivering ceria and Ac2-26 peptide for penumbra protection in ischemic stroke. 模拟巨噬细胞脂质体共同递送铈和Ac2-26肽对缺血性脑卒中的半暗区保护作用。

IF 10.6 1区生物学

Journal of Nanobiotechnology Pub Date : 2025-07-05 DOI: 10.1186/s12951-025-03575-9

Lingyun Bai, Na Li, Huiqin Li, Yuxuan Dai, Yi Bai, Feiyu Ma, Dujuan Sha, Shengnan Xia, Yun Xu, Xiang Cao

{"title":"Macrophage-mimetic liposomes co-delivering ceria and Ac2-26 peptide for penumbra protection in ischemic stroke.","authors":"Lingyun Bai, Na Li, Huiqin Li, Yuxuan Dai, Yi Bai, Feiyu Ma, Dujuan Sha, Shengnan Xia, Yun Xu, Xiang Cao","doi":"10.1186/s12951-025-03575-9","DOIUrl":"10.1186/s12951-025-03575-9","url":null,"abstract":"Ischemic stroke is one of the most severe central nervous system disease with high disability and mortality rates worldwide. Effective treatment requires strategies that address the multifaceted pathophysiology of ischemic penumbra, including oxidative stress-induced neuronal apoptosis and blood-brain barrier (BBB) disruption. Here, inspired by the inflammation-homing property of macrophages, we developed macrophage-mimetic liposomes (MM-LPs) by integrating macrophage membranes with liposomes for the co-delivery of cerium oxide nanoparticles (CeO2) and the Ac2-26 peptide (CeO2-Ac2-26@MM-LPs). CeO2 effectively scavenged reactive oxygen species (ROS), improving mitochondrial function and inhibiting neuronal apoptosis, while Ac2-26 upregulated tight junction proteins to enhance BBB integrity. In a transient middle cerebral artery occlusion (tMCAO) mouse model, CeO2-Ac2-26@MM-LPs exhibited significant accumulation in ischemic regions, where they exerted dual protective effects on the ischemic penumbra by mitigating neuronal damage and preserving BBB integrity. This resulted in improved neurological function, reduced infarct volume, and attenuated BBB disruption. Mechanistically, CeO2-Ac2-26@MM-LPs activated the NRF2 signaling pathway, upregulating antioxidant enzymes (HO-1 and NQO1), while simultaneously suppressing NF-κB activation, thereby reducing neuronal death and BBB damage in the penumbra. This multi-target combination strategy provides a promising platform for ischemic stroke treatment, with potential applicability to other neurological disorders characterized by oxidative stress and BBB disruption.","PeriodicalId":16383,"journal":{"name":"Journal of Nanobiotechnology","volume":"23 1","pages":"488"},"PeriodicalIF":10.6,"publicationDate":"2025-07-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12228292/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144567529","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}

引用次数: 0