JOURNAL OF NANOBIOTECHNOLOGY
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2026
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IF 15
Tu Maopu,Deng Xiaoyu,Zhou Zhiyong,Li Xiaodong,Mao Shengxun,Lai Bin,Pang Lisong,Zhong Qilin,Cao Jiaqing,Liu Haipeng,Ouyang Xi
Microsatellite-stable (MSS) colorectal cancer (CRC) resists immunotherapy due to its immunosuppressive tumor microenvironment (TME). The cGAS-STING pathway, a key regulator of innate immunity, offers a promising strategy to overcome the immunotherapy resistance in CRC. However, its limited endogenous activation, coupled with the immunosuppression driven by lactate accumulation, significantly compromises the efficacy of standalone STING activation. In response, we developed a multifunctional copper-based metal-organic framework (Cu-MOF) nanoparticle co-loaded with the STING agonist SR-717 and the glycolysis inhibitor 3-bromopyruvate (3-BP), coated with tumor cell membranes (termed BR@CuM@CM), to achieve integrated metabolic modulation and immune activation. BR@CuM@CM nanoparticle achieves tumor-specific accumulation via homotypic targeting and undergo glutathione-responsive degradation to trigger drug release. The released SR-717 activates the STING pathway, promoting dendritic cell (DC) maturation and thereby enhancing cytotoxic T-cell recruitment. Concurrently, Cu²⁺ triggers Fenton-like reactions to generate reactive oxygen species (ROS), inducing mitochondrial DNA release and further amplifying STING signaling. Meanwhile, 3-BP suppresses lactate production by inhibiting glycolysis, which not only repolarizes M2-type tumor-associated macrophages toward the M1 phenotypes and suppresses regulatory T cell (Treg) infiltration, but also alleviates cGAS lactylation to enhance cGAS activity and amplifying STING-mediated immune responses. When combined with anti-PD-1, the nanoparticle significantly inhibits tumor growth and liver metastasis. Collectively, BR@CuM@CM synergistically modulates metabolism and immune signaling to convert immunologically “cold” tumors into “hot” tumors, demonstrating translational potential to overcome immunotherapy resistance in CRC. Graphical
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高影响因子
NEUROCHEMICAL RESEARCH
·
2026
·Vol. 51
·期 2
·94
·
IF 4.5
Lin Yang,Zhang Kun,Zhang Meijie,Yin Lida,Liu Zhixin,Meng Yanru,Li Yue,Meng Jinhui,Yin Xueyong,Wang Liping
VCAN-AS1 is a novel long non-coding RNA that participates in diverse disease processes, but the mechanism of its action in cerebral infarction secondary epilepsy (CISE) is unclear. The potential action mechanism of VCAN-AS1 in CISE was explored by this study. VCAN-AS1 and its downstream targets, namely miR-885-3p and Netrin G1 (NTNG1), were screened by the GEO, LncRNASNP2, and miRDB databases. The epileptic mouse and cell models were constructed using pilocarpine and the Mg 2+ -free medium, respectively. ELISA kits or RT-qPCR was used for the measurement of TNF-α/IL-1/IL-6 levels. The levels of Fe 2+ , GSH, and ROS were detected by the specific biochemical kits. GPX4 expression was analyzed by RT-qPCR. Dual-luciferase reporter assay was used to detect the interactions between miR-885-3p and VCAN-AS1 or NTNG1. Meanwhile, the expression levels of VCAN-AS1, miR-885-3p, and NTNG1 were detected by RT-qPCR. Elevated serum levels of VCAN-AS1 were observed in patients with CISE, and silencing of VCAN-AS1 attenuated inflammation and ferroptosis in epilepsy-associated neurons and the hippocampus of epileptic mice. VCAN-AS1 negatively regulated miR-885-3p which subsequently repressed NTNG1 expression. Up-regulation of miR-885-3p inhibited inflammation and ferroptosis in epileptic mouse and cell models, and overexpression of NTNG1 reversed these effects of miR-885-3p. The suppression of VCAN-AS1 expression mitigated neuronal inflammation and ferroptosis in epileptic conditions by targeting the miR-885-3p/NTNG1 regulatory axis, which may be an important molecular mechanism of CISE.
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MOLECULAR NEUROBIOLOGY
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2026
·Vol. 63
·期 1
·467
·
IF 5.5
Zhang Bin,Bian Weiming,Zhu Kaiyuan,Dai Yuzhen,Cai Miao,Cheng Jiaqi,Chen Xinyan,Xiang Zheng,Liu Yixiu,Lu Wen
Alzheimer's disease (AD) is a prevalent neurodegenerative disorder characterized by cognitive decline and neuropsychiatric symptoms, among which impaired fear responses are particularly notable. While studies have established that learned fear is compromised in AD, the status of innate fear in this context remains unclear. We found that young adult female APP/PS1 mice exhibited reduced freezing and avoidance responses to 2,5-dihydro-2,4,5-trimethylthiazoline (TMT) compared to their wild-type littermates, indicating an impaired innate fear response. Additionally, c-Fos-positive cells in the basolateral amygdala (BLA), a key region for fear processing, were significantly lower in the APP/PS1 mice. Notably, metformin treatment significantly restored TMT-induced freezing behavior and increased c-Fos-positive cells in the BLA, suggesting that it can reverse the innate fear deficit in this AD model. Mechanistically, chemogenetic inactivation of the BLA abolished the therapeutic effects of metformin on the innate fear deficit. Our study suggests metformin as a promising candidate for therapeutic intervention aimed at improving innate fear-related behavioral deficits in AD.
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WATER AIR AND SOIL POLLUTION
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2026
·Vol. 237
·期 11
·638
·
IF 3.5
Peng Xue,Zhang Xinyi,Zhang Shuxian,Lin Qingwei,Zhang Haokun,Zhang Xiaowen,Zhang Yi,Xu Steven Jing-Liang,Lee Fred Wang-Fat,Tam Nora Fung-yee,Wu Zhenbin,Liu Biyun
The widespread use of aluminum-based coagulants in ecological restoration projects has raised increasing concerns regarding the potential ecological impacts of residual aluminum (Al) in aquatic ecosystems. Epiphytic biofilms on submerged plants play a vital role in regulating nutrient cycling and energy flow in aquatic environments. However, the effects of Al on the biological and abiotic components of epiphytic biofilms on submerged macrophyte leaves remain poorly understood. In this study, we investigated the Al content in epiphytic biofilms on Vallisneria natans and its relationships with nitrogen, phosphorus and bacterial composition in Hangzhou West Lake, China. This location was selected due to the potential for residual Al into the lake from the daily pretreatment of the Qiantang River water diversion project—a water quality improvement project. Our results showed that Al contents in epiphytic biofilms decreased with increasing distance from the inlet and were positively correlated with total phosphorus, Chlorophyll-a and ash-free dry mass ( P < 0.05), but showed no significant correlation with total nitrogen. Al accumulation enhanced Chl-a levels in biofilms by increasing the inorganic phosphorus content. Furthermore, Al content was positively correlated with the abundance of Cyanobacteria and negatively correlated with the abundance of Proteobacteria. Al also showed a significant negative correlation with key denitrifying bacteria, such as Vogesella and Phreatobact er, suggesting that elevated Al levels might affect the nitrogen cycling function in epiphytic biofilms. These findings provide important reference data for for ecological risk assessment and inform management strategies for aquatic systems undergoing restoration or exposed to aluminum-based treatments. Graphical
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BIOLOGICAL TRACE ELEMENT RESEARCH
·
2026
·
IF 4.3
Abbas Mubbashar,Suliman Khan,Chen Min,Ying Zhao,Ashaq Muhammad Sameer,Asif Ali,Khan Muhammad Ali,Chen Dongmei,Xie Shuyu
Ulcerative colitis (UC) is characterized by excessive cytokine production, epithelial barrier disruption, and oxidative stress. It necessitates therapeutics with immunomodulation and mucosal integrity restoration. This study aimed to evaluate in-vivo and in-vitro therapeutic potential of Fe-MOF, Cr-MOF, and Co-MOF. RAW264.7 macrophages and DSS-induced murine colitis model were used. SEM, FTIR, XRD, and ICP-MS were used for characterization of MOFs. Cytotoxicity, immunofluorescence, ELISA, histopathology, immunoblotting, and qPCR analyses were used to evaluate effects of MOFs. Co-MOF showed a significant immunomodulatory effect by reducing LPS-induced TNF-α, IL-6, and IL-1β expression at both mRNA and protein levels in RAW264.7 macrophages. It also alleviated DSS-induced TNF-α, IL-6, and IL-1β levels in mouse colon, as indicated by ELISA and immunofluorescence. Co-MOF also reduced DAI score, improved body weight loss, and preserved colon length in the DSS-induced colitis model. Co-MOF also restored tight-junction proteins such as Occludin and ZO-1, significantly reduced by DSS in colon. Histopathological examination validated substantial protection of mucosal architecture, including intact crypts, restored goblet cell populations, and attenuated immune-cell infiltration. A notable antioxidant effect of Co-MOF was also observed, as it increases SOD and CAT activities while reducing MDA. Co-MOF significantly normalized platelets, lymphocytes, and neutrophils, elevated by DSS. Co-MOFs did not induce systemic toxicity and vital organ injury, predicting their biosafety. Conclusively, Co-MOF showed better immunomodulatory effects and barrier protection compared to Fe-MOF and Cr-MOF in UC, which further requires mechanistic validation.
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Nature Communications
·
2026
·
IF 18.1
Shaojie Chen,Hao Tang,Xiaoliang Fan,Bohan Li,Yaomin Wang,Wei Zhou,Xiaoyu Jiang,Xiaomin Dong,Yanyi Wang,Peng Zhao,Tianwen Ye,Bolin An,Yijun Zheng,Chao Zhong
Bacterial cellulose possesses excellent biocompatibility and mechanical strength but lacks the bioactivity needed for many biomedical and healthcare applications. To address this limitation, we develop a metabolic glycoengineering–click chemistry strategy that enables in situ incorporation of azide groups into bacterial cellulose, followed by mild and selective conjugation of alkyne-bearing functional molecules. This approach avoids harsh chemical treatments, preserves the native properties of bacterial cellulose, and supports stable attachment of diverse bioactive agents, including antibacterial porphyrins, arginine-glycine-aspartic acid peptides, and recombinant proteins with fluorescent or enzymatic functions. As a proof-of-concept, a cascade catalytic system comprising glucose oxidase and superoxide dismutase is immobilized onto azide-modified bacterial cellulose, yielding a multifunctional wound dressing designed to address hyperglycemia and oxidative stress—key barriers to chronic wound healing. In male diabetic mice, this glucose oxidase/superoxide dismutase-integrated bacterial cellulose dressing (low endotoxin <0.1 EU/mL) accelerates wound closure to 92.1% by day 14, significantly outperforming the controls. Our strategy highlights a scalable and bio-orthogonal route for enhancing bacterial cellulose with user-defined bioactivities, thereby expanding its utility in advanced biomaterials development. Bacterial cellulose (BC) possesses excellent biocompatibility and mechanical strength but lacks the bioactivity needed for many biomedical applications. Here the authors use glycoengineering–click chemistry to incorporate azide groups into BC in situ, and show enhanced BC-mediated wound healing.
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CELL DEATH AND DIFFERENTIATION
·
2026
·
IF 13.6
Li Yitao,Zheng Weijia,Ma Jiao,Liu Lu,Yang Xintong,Kuang Junliang,Chan Nickie,Wang Chengqiang,Li Yang,Zhao Aihua,Wang Ruonan,Zheng Xiaojiao,Melino Gerry,Lu Aiping,Yang Xiaolu,Jia Wei
Autoimmune uveitis (AU) lacks targeted therapies beyond immunosuppression. We identified hyodeoxycholate (HDCA), a gut-derived secondary bile acid, as a key immunometabolic regulator in AU. Metabolomics revealed systemic depletion of HDCA and oleic acid (C18:1n9) in AU patients and experimental AU (EAU) mice, correlating with disease severity. HDCA administration effectively attenuated EAU by reducing pro-inflammatory cytokines (IL-1β, IL-6, and TNF-α) and elevating IL-10. Mechanistically, HDCA inhibits Farnesoid X Receptor in splenic red pulp macrophages, activating SREBP1c-dependent fatty acid synthase, which enhances oleic acid production. Systemic oleic acid suppresses ocular Th17 responses and promotes M2 macrophage polarization, enhancing anti-inflammatory immunity. These findings define a spleen-to-eye immunometabolic axis driven by HDCA-mediated macrophage reprogramming, positioning HDCA as a promising therapeutic for AU.
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JOURNAL OF NANOBIOTECHNOLOGY
·
2026
·
IF 15
Ma Tianyu,Li Qiang,Chen Xingwu,Dong Jixiang,Jiang Yuqing,Li Shanshan
Bioactive peptides are promising candidates for hair regeneration, but their topical application is often limited by poor skin delivery and the need for frequent dosing. To overcome these challenges, we designed a palmitoylated peptide, Pal-MPAPO, and incorporated it into a hyaluronic acid-based hydrogel microneedle (MN) system for localized transdermal delivery. The fabricated MNs showed adequate mechanical strength for skin insertion and provided a time-dependent, prolonged release of Pal-MPAPO. In human dermal papilla cells (DPCs), Pal-MPAPO activated the Wnt/β-catenin pathway and increased intracellular cyclic adenosine monophosphate (cAMP) levels in a predominantly VPAC1-dependent manner. Additional VPAC2 validation did not reveal a significant contribution to cAMP signaling under the tested conditions. Functional interactions between Pal-MPAPO and VPAC1 were supported by molecular docking, molecular dynamics simulations, receptor knockdown, and fluorescence imaging. In a C57BL/6 mouse model, Pal-MPAPO-loaded MNs significantly promoted hair regrowth, achieving efficacy comparable to minoxidil but at a reduced application frequency. These findings identify Pal-MPAPO as a potential peptide candidate for hair regeneration and suggest that hydrogel MN-assisted delivery provides a localized peptide administration strategy. Graphical The alternative text for this image may have been generated using AI.
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Journal of Animal Science and Biotechnology
·
2026
·Vol. 17
·期 1
·109
·
IF 7.9
Zhang Jiaqi,Shi Xiaohan,Peng Siyi,Zhang Chi,Qiao Shiyan,Yu Haitao
Background While the livestock industry actively seeks alternatives to antibiotics, residual low-dose exposures continue to drive the spread of antibiotic resistance genes (ARGs). Icariin, a plant-derived compound, is recognized for improving poultry growth and immunity. However, it remains unclear how this compound influences the environmental persistence of ARGs, mobile genetic elements (MGEs), and horizontal gene transfer (HGT) during the vulnerable recovery phase after antibiotic withdrawal. Results We designed a two-phase feeding trial with laying hens, using longitudinal metagenomic sequencing to track post-withdrawal resistance dynamics. Following initial exposure to a low-dose antibiotic mixture that established a baseline of elevated resistance, hens received either a basal diet, an icariin-supplemented diet, or a copper sulfate-supplemented diet. The data indicate that icariin supplementation consistently reduced the burdens of both ARGs and MGEs. It also suppressed the potential for HGT and restricted the diversity of microbial hosts harboring these resistance elements. Conversely, copper sulfate—a traditional metal-based additive—exacerbated resistance risks by expanding both the abundance and the host range of ARGs and MGEs. Across all treatments, the population of Escherichia and the prevalent ARG subtype bacA correlated strongly with total resistance loads, tracking the overall resistome burden. Conclusions Compared to conventional copper sulfate treatments, icariin facilitates a safer ecological recovery in the poultry gut by actively lowering ARG and MGE reservoirs after antibiotic withdrawal. These genomic insights, combined with its known physiological benefits, support icariin as a sustainable feed additive. Furthermore, the Escherichia - bacA correlation provides a reliable, streamlined indicator for monitoring resistance risks in farm environments. However, as these findings rely on short-term fecal metagenomic tracking, further validation through multi-environment studies is warranted. Graphical
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BMC MICROBIOLOGY
·
2026
·
IF 5.4
Hao Danrui,Huang Yuhang,Zhao Tianzhu,Wang Runyu,Jiang Wei,Yuan Xiangting,Wang Xinrong,Chu Yiwen,Zhao Kelei,Huang Ting,Wang Zhenxing
Background Acinetobacter baumannii is a notorious clinical pathogen that predominantly causes nosocomial infections. The multidrug resistant Acinetobacter baumannii clinical isolates are becoming more prevalent on a global scale. In this study, we aimed to determine the potential synergistic antibacterial activity of contezolid in combination with polymyxin B nonapeptide (PBNP) against various A. baumannii strains. Results Contezolid, a commonly-used agents targeting Gram-positive bacteria, in combination with PBNP (CP) was used to explore the potential synergistic antibacterial activity against A. baumannii in vitro and Caenorhabditis elegans models. We found that CP treatment exhibited a strong synergistic effect on A. baumannii or multidrug resistant A. baumannii . CP also inhibited the biofilm formation and alter morphology of A. baumannii compared to the control group. Moreover, the residual bacteria were significantly decreased in the CP-treated murine alveolar macrophages (MH-S). Importantly, CP treatment improved the survival of C. elegans compared to the control or monotherapy group. Conclusions This strategy improved antibacterial activity spectrum of agents targeting Gram-positive bacteria like contezolid. Nevertheless, CP combination therapy requires further validation in mammalian infection models.
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JOURNAL OF NANOBIOTECHNOLOGY
·
2026
·
IF 15
Yao Jing,Li Yanyan,Meng Yiling,Wang Tao,Meng Jie,Liu Jian,Wen Tao,Xu Haiyan
Acute myeloid leukemia (AML) is characterized by differentiation arrest and apoptosis resistance, frequently with mitochondrial dysfunction and aberrant heat shock protein 60 (HSP60) overexpression as key drivers of malignant progression. Platinum-based nanozymes exhibit multi-enzymatic activity but lack organelle specificity, limiting their therapy efficacy. Based on that there are abundant HSP60 in mitochondrial, we constructed a peptide-conjugated nanozyme PtNPs-P17 by conjugation platinum nanoparticle (PtNPs) and HSP60-targeting peptide P17. It was shown that PtNPs-P17 retained intrinsic oxidase (OXD), peroxidase (POD), superoxide dismutase (SOD), and catalase (CAT)-like activities while acquiring the targeting ability. In the myeloperoxidase (MPO)-positive AML cell line MOLM-13, PtNPs-P17 specifically localized to mitochondria in cells, significantly increasing the production of reactive oxygen species (ROS), oxygen and especially singlet oxygen due to its multi-enzymatic redox regulatory function, which disrupted mitochondrial membrane potential and triggered mitophagy evidenced by the elevated LC3BII/actin ratio and LC3B-mitochondria co-localization. Moreover, PtNPs-P17 induced dual inhibition of mitochondrial respiration and glycolysis, leading to total NAD levels reduced. These metabolic perturbations together resulted in the differentiation of the AML cells, with up-regulated levels of CD235a, CD11b, and CD41a, and enhanced apoptosis. In a refractory AML mouse model, PtNPs-P17 significantly down-regulated the HSP60 expression while reduced spleen GFP + leukemia cells, suggesting significantly enhanced anti-leukemia effects compared to PtNPs. In conclusion, it was demonstrated that PtNPs-P17 targeted mitochondrial HSP60 to induce mitophagy by orchestrating multi-enzymatic redox regulation and mitochondrial reprogramming, thereby overcoming AML differentiation block and apoptosis resistance. This study provides a novel AML therapy option via precise mitochondrial targeting and metabolic intervention, highlighting the translational potential of HSP60-targeted multi-enzyme nanozymes. Graphical abstract The alternative text for this image may have been generated using AI.
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高影响因子
JOURNAL OF NANOBIOTECHNOLOGY
·
2026
·Vol. 24
·期 1
·464
·
IF 15
Wang Xueqing,Li Kai,Xu Wenyan,Wang Danyang,Wang Ying,Feng Junkun,Chen Yi,Liu Xiaoyi,Xu Zishan,Liu Xiaojia,Ge Shaohua,Liu Hong,Li Jianhua
Osteomyelitis is a refractory bacterial infection of bone, presenting significant clinical management challenges due to its limited therapeutic outcome. Here, we developed heterojunction-structured sub-1 nm copper oxide-decorated strontium titanate nanosheets (Cu-STO NSs), which integrate piezocatalytic reactive oxygen species (ROS) generation with augmented copper-induced bacterial death for synergistic osteomyelitis treatment. Under ultrasound (US) irradiation, the oxygen vacancies and heterojunction structure of Cu-STO NSs facilitate the separation of piezo-generated electron–hole pairs while reducing energy barriers, thereby enhancing ROS generation. This process is augmented by the US-accelerated Cu 2+ /Cu + redox cycling, which enables sustained hydroxyl radicals supply via Fenton-like reactions. The US-driven piezocatalytic action simultaneously enhances bacterial membrane permeability, facilitating intracellular copper overload and thereby triggering copper-induced metabolic toxicity in Staphylococcus aureus ( S. aureus ). Subsequent release of bioactive Cu and Sr ions from Cu-STO NSs significantly upregulates osteogenic differentiation of bone marrow stromal cells. In rat osteomyelitis, Cu-STO NSs achieve efficient bacterial eradication while stimulating on-demand bone regeneration. This work thus presents a non-invasive, spatiotemporal controlled copper-induced bacterial death strategy that concurrently addresses antibacterial and osteogenic challenges in infected bone regeneration. Graphical The alternative text for this image may have been generated using AI.
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