Advanced Sensor and Energy Materials
·
2026
·
IF 12.3
Tingting Wang,Hao Song,Xiaohui Gong,Zongyu Han,Taoming Xu,Yanan Xu,Dan Zhao,Chuanxia Chen,Yizhong Lu,Jian Sun
Biothiol analysis is crucial for evaluating redox homeostasis and monitoring various physiological processes. However, conventional fluorescence-based strategies often rely on structurally complex probes and lack straightforward multi-target discriminative capabilities. Herein, we present a versatile, pre-synthesis-free fluorogenic platform driven by the target-responsive inhibition of in-situ polymer dot (PD) formation. We discovered that dopamine (DA) spontaneously condenses with N -[3-(trimethoxysilyl)propyl]diethylenetriamine (AEEA) to yield robustly fluorescent PDs. Biothiols, acting as highly reactive competitors, intercept the DA precursor via a preferential Michael addition, fundamentally suppressing PD formation and inducing a marked fluorescence decrease. This mechanism enables the rapid, highly sensitive quantification of glutathione (GSH), cysteine (Cys), and homocysteine (Hcy), with low limits of detection (LODs) of 0.095, 0.115, and 0.083 μM, respectively. Significantly, the introduction of a structurally distinct DA-DAMO analog facilitated the discrimination of these biothiols. This reaction-interference strategy was then successfully coupled with enzymatic cascades to evaluate glutathione reductase (GR) activity within 20 min, achieving a LOD of 0.046 mU/mL. The programmable analyte-dependent fluorescence outputs were successfully employed as signal readouts to construct molecular logic gates. This work establishes target-regulated in-situ nanomaterial formation as a powerful paradigm for biothiol sensing, enzyme assays, and advanced logic operations.
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Sustainable Materials and Technologies
·
2026
·
IF 9.7
XiaoPu Dong,Xinzhou Wu,Wanting Huang,Qiyu Liu,Xueqing Qiu,Jinhao Huang,Dafeng Zheng
Biomass-based aerogels derived from polysaccharides and proteins have attracted considerable interest because of their environmental compatibility, cost-effectiveness, and inherent biodegradability. However, their carbon- and hydrogen-rich chemical structures render them intrinsically flammable, necessitating effective flame-retardant modification to satisfy stringent fire-safety requirements. Herein, an eco-sustainable strategy is reported for constructing biomass-derived composite aerogels that simultaneously integrate high mechanical strength, efficient thermal insulation, and enhanced fire safety. High-strength flame-retardant aerogels were fabricated from sodium alginate (SA), sodium lignosulphonate (LS), and hydroxyapatite (HAP) through a glucono-δ-lactone (GDL)-regulated in situ ion-release strategy. The gradual hydrolysis of GDL induces controlled acidification of the precursor system, promoting the sustained release of Ca 2+ from HAP and the homogeneous ionic cross-linking of SA chains into a stable three-dimensional “egg-box” network. The mechanically optimized SL3H0.6G0.8 aerogel achieved the highest compressive modulus of 9.32 MPa, corresponding to approximately 13 times that of pristine SA aerogel (0.69 MPa). In contrast, SL3H0.9G0.8 exhibited the most balanced overall performance, retaining a lightweight porous structure and a low axial thermal conductivity of 0.04553 W m −1 K −1 while delivering superior thermal stability, flame retardancy, and smoke-suppression capability. The enhanced fire resistance originates predominantly from a synergistic condensed-phase mechanism involving LS-derived carbonaceous char formation, phosphate-assisted dehydration and carbonisation, and reinforcement by thermally stable calcium/phosphate-rich inorganic residues. The resulting organic-inorganic protective layer effectively suppresses heat transfer, volatile release, and smoke evolution during combustion. Consequently, SL3H0.9G0.8 achieved a UL-94 V-0 rating and a limiting oxygen index of 37.5%, together with a peak heat release rate of 104.56 W g −1 and a total smoke production of 0.23 m 2 . This work establishes a sustainable route for the green fabrication of mechanically robust, thermally insulating, and fire-safe biomass-based aerogels, offering considerable potential for energy-efficient building applications.
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BIORESOURCE TECHNOLOGY
·
2026
·
IF 8.2
Licong Xu,Cunxu Gong,Minghua Wu,Deyou Yu
Waste sericin was valorized into Fe 3 O 4 / N -doped porous biochar Fenton-like catalyst. • Molecular coordination enabled uniform dispersion of active Fe 3 O 4 nanoparticles. • 0.1Fe-NC degraded 99.3% AO-7 with kobs of 0.266 min −1 via PMS activation. • Multiple ROS including Fe(IV)=O and 1 O 2 dominated the reaction. • Packed-bed continuous-flow operation kept >98% AO-7 removal for 720 min. Developing sustainable catalysts from waste biomass for advanced oxidation processes is highly desirable for wastewater treatment. Herein, a waste-to-resource strategy was proposed to upcycle silk-industry waste sericin into Fe 3 O 4 -anchored N -doped porous biochar Fenton-like catalysts (Fe-NC) for peroxymonosulfate (PMS) activation. Distinct from conventional biomass-derived Fe/carbon catalysts that often require external nitrogen dopants or post-loading of metal species, sericin served simultaneously as a carbon source, intrinsic nitrogen precursor, and Fe 3+ -binding biopolymer, enabling the coordination-assisted formation of Fe 3 O 4 / N -doped carbon interfacial active sites after controlled pyrolysis. The optimized 0.1Fe-NC possessed a high specific surface area of 477.9 m 2 g −1 and uniformly dispersed Fe 3 O 4 nanoparticles, enabling rapid removal of Acid Orange 7 (AO-7) over a wide pH range of 4–11. Nearly complete degradation of AO-7 (99.3%) was achieved within 30 min, with a pseudo-first-order rate constant ( k obs ) of 0.266 min −1 . Mechanistic investigations revealed that multiple reactive oxygen species, including Fe(IV)=O, SO 4 -, OH, and 1 O 2 , jointly contributed to pollutant degradation. In addition, the catalyst exhibited excellent magnetic recoverability and stability, maintaining 89.7% removal efficiency after five cycles. Continuous-flow experiments further demonstrated stable performance (>98% removal for 720 min), highlighting its practical applicability. This work provides a sustainable strategy for converting protein-rich sericin waste into efficient Fe-based biochar catalysts and offers insights into designing biomass-derived PMS activation systems with integrated heteroatom doping, metal anchoring, and interfacial electron-transfer regulation. Download: Download high-res image (166KB) Download: Download full-size image
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高影响因子
Journal of the American Chemical Society
·
2026
·Vol. 148
·期 29
·31263-31280
·
IF 16.6
Ouyang Fangyan,Xiong Huihuang,Ding Dan,Wan Yiqun,Liu Minhai,Liang Yongye,Dai Hongjie,Wan Hao
It has been highly challenging to
reliably detect various
cancers
at an early stage when tumors are just millimeters in size. To address
this, we developed a tumor microenvironment (TME)-responsive nanoprobe,
PR-KAd@CD-AuNC, enabling cross-validated cancer detection through in vivo second near-infrared (NIR-II) fluorescence imaging
and in vitro colorimetric urinalysis. The nanoprobe
consists of three integrated components: a renal-clearable signal-output
segment (cyclodextrin-functionalized gold nanocluster, CD-AuNC), a
tumor-targeting and size-controlling component (PR), and a matrix
metalloproteinase-2 (MMP2)-cleavable linker (KAd). PR, composed of
8-arm poly(ethylene glycol) for prolonged circulation and c(RGDfK)
peptides for α v β 3 integrin targeting,
directed selective tumor accumulation after intravenous injection
of PR-KAd@CD-AuNC. The intrinsic emission of CD-AuNC above 1100 nm
enabled high-resolution, real-time NIR-II fluorescence imaging with
attenuated photon scattering, allowing precise tumor delineation.
Within the TME, specifically overexpressed MMP2 cleaved the KAd linker,
releasing ∼2 nm CD-AuNC fragments from the ∼10 nm parent
nanoprobe. Being smaller than the ∼5.5 nm renal filtration
threshold, these fragments were renally excreted. Concurrently, the
peroxidase-like activity of CD-AuNC catalyzed tetramethylbenzidine
oxidation to produce a visible blue signal, providing a simple and
low-cost urinalysis method suitable for broad cancer screening applications.
This dual-modality strategy effectively distinguished cancers from
inflammation and other diseases, detecting small tumors for multiple
cancer types with a sensitivity surpassing that of computed tomography
(CT) imaging, which makes it a promising early detection approach.
Furthermore, it was also employed to dynamically assess cancer therapeutic
efficacy (i.e., immunotherapy, chemotherapy, and surgical resection),
suggesting clinical value for guiding treatment decisions.
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Materials Today Bio
·
2026
·
IF 11
Huaze Ding,Xinhui Huang,Peng Hu,Xiaoyan Zhang,Yulin Wang,Baiwei Mao,Jianxin Ye,Dianwen Song,Chong Zhang,Changping Wang
Acute kidney injury (AKI) represents a critical medical condition with high mortality and no effective pharmacotherapy. Mitochondrial dysfunction in proximal tubular epithelial cells (PTECs), characterized by NAD + depletion, CoQ oxidation, and reactive oxygen species (ROS) overproduction, is a central driver of tubular damage and maladaptive repair. As central metabolic molecules, NAD + and CoQ can effectively ameliorate acute kidney injury by alleviating mitochondrial oxidative stress. However, the bioavailability of NAD + is limited by its short half-life, instability, and poor membrane permeability, whereas CoQ, despite being lipophilic, lacks specific mitochondrial targeting, preventing maximal therapeutic efficacy. Here, we report carrier-free NAD + /MitoQH 2 nanoparticles (NM NPs) with ultrasmall size and ROS-responsive properties. NM NPs are designed to pass through the glomerular filtration barrier and preferentially accumulate in injured renal tubules, where they may replenish the NAD + pool and provide a pre-reduced, mitochondria-targeted ubiquinol to support the CoQ axis under oxidative stress. Through renal accumulation and ROS-responsive release, NM NPs showed therapeutic efficacy in hypoxia/reoxygenation- and cisplatin-induced AKI models, as evidenced by reduced ROS accumulation, improved mitochondrial oxidative phosphorylation, enhanced autophagy, and attenuated ferroptosis. This work presents a metabolic nanomedicine strategy based on the co-assembly of bioactive molecules to modulate the mitochondrial NAD + –CoQ axis, providing a promising platform for AKI therapy and potentially other mitochondria-associated diseases.
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CHEMICAL ENGINEERING JOURNAL
·
2026
·
IF 12.5
Zihan Liu,Jiale Miao,Weiqing Ni,Ting Yang,Wenjing Dong,Junjiang Yu,Jiayu Yang,Yanhua Liu
An inflammation-responsive and endothelial cell-targeting R/HTM prodrug micelle nanotherapeutic system was developed for the effective management of rheumatoid arthritis. • R/HTM micelles realized dual modulation of neutrophil recruitment and survival via blocking P-selectin/PSGL-1-mediated adhesion cascade and ROS-triggered site-specific co-release of R-rsc and methylprednisolone. • R/HTM micelles comprehensively regulated the pathological synovial microenvironment, including clearing excess ROS, and inhibiting fibroblast-like synoviocyte invasion. • R/HTM micelles markedly mitigated synovial inflammation, cartilage damage and bone erosion in AIA rat models, holding broad translational potential for neutrophil-dominated inflammatory diseases. Rheumatoid arthritis (RA) is a chronic autoimmune disease characterized by persistent synovial inflammation and progressive joint destruction, wherein aberrant neutrophil infiltration and prolonged neutrophil survival drive the amplification of inflammatory cascades. To disrupt these pathological processes, an inflammation-responsive, endothelial cell-targeting nanotherapeutic platform was constructed for dual modulation of neutrophil recruitment and survival. This system is composed of a heparin-thioketal-methylprednisolone (HTM) prodrug that self-assembles into HTM micelles, and it is loaded with the cyclin-dependent kinase inhibitor R-roscovitine (R-rsc) to produce R/HTM (R-rsc/HTM micelles). R/HTM micelle treatment effectively inhibited neutrophil recruitment in vitro by blocking P-selectin/PSGL-1-mediated adhesion to inflamed vascular endothelial cells. In the reactive oxygen species-enriched joint synovial microenvironment of the adjuvant-induced arthritis rat model, R/HTM micelle disassembly enabled co-release of R-rsc and methylprednisolone, which synergistically induced neutrophil apoptosis through Bcl-2 downregulation and Bax/Caspase-3 upregulation. This dual-phase strategy also suppressed neutrophil extracellular trap formation, reprogrammed macrophage polarization (toward an anti-inflammatory M2 phenotype), inhibited fibroblast-like synoviocyte invasion, and cleared excess ROS. Moreover, R/HTM treatment significantly alleviated joint inflammation, repaired cartilage damage, ameliorated bone erosion, and suppressed the levels of pro-inflammatory cytokines (IL-6, IL-1β and TNF-α). Collectively, these findings establish R/HTM micelles as a potent nanotherapeutic system with a dual-phase mechanism that targets the key pathological checkpoints of neutrophil-mediated inflammation, offering a promising approach for the effective management of RA.
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COLLOIDS AND SURFACES B-BIOINTERFACES
·
2026
·
IF 5.9
Zhengjie Meng,Ziyan Wang,Chenyu Lu,Fei Xue,Luming Huang,Hengjian Wang,Dong Wang,Jing Yang,Jiang Tian,Chenyu Ma,Yunhao Bai,Yonglu Wang,Xueming Li,Hao Ren,Qiyue Wang
Nephritis-responsive dual-targeting HA-modified hollow mesoporous polydopamine nanoparticles for AKI combination therapy. • An all-in-one kidney-targeted system jointly alleviates oxidative stress, inflammation, and immune dysregulation. • The all-in-one system improves flavonoid solubility, bioavailability, and targeting, boosting efficacy and reducing toxicity. Acute kidney injury (AKI) is a severe syndrome driven by oxidative stress and inflammation, with limited effective drug therapy. Total flavonoids (Fla) from Abelmoschus manihot (L.) Medic have strong antioxidant and anti-inflammatory activity, but poor solubility and weak renal targeting limit its clinical translation. Here, a nephritis microenvironment-responsive dual-targeting nanoplatform (Fla@HMPDA@HA) was constructed by loading Fla into hyaluronic acid (HA)-modified hollow mesoporous polydopamine (HMPDA) nanoparticles. HMPDA provided high drug-loading capacity and intrinsic reactive oxygen species (ROS)-scavenging activity, enabling a synergistic therapeutic effect with Fla. Fla@HMPDA@HA could be efficiently internalized by injured renal tubular epithelial cells, reversed H 2 O 2 -induced oxidative injury, restored mitochondrial membrane potential, and reduced apoptosis. It also promoted macrophage polarization from an M1-like to an M2-like phenotype up to 43.35%, while significantly downregulating TNF-α, IL-6, and IL-1β. In vivo imaging confirmed preferential accumulation of HA-modified nanoparticles in damaged kidneys. After intravenous administration, Fla@HMPDA@HA preserved kidney structure, restored renal function, and alleviated local inflammation and apoptosis, thereby markedly attenuating LPS-induced AKI with negligible systemic toxicity. Overall, this dual-targeting platform integrates targeted delivery, anti-inflammatory activity, and immune microenvironment remodeling together, offering a promising therapeutic strategy for AKI.
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Acta Biomaterialia
·
2026
·
IF 10.4
Mengxing Lu,Yongan Lin,Dawei Qi,Baolei Huang,Ye Tian,Shasha Gao,Zhuhao Tan,Qihui Lin,Dan Ying,Wenfang Liu,Wenjing Song,Li Ren
Dry eye disease (DED) is a multifactorial ocular surface disorder driven by tear film instability, excessive evaporation, frictional damage, oxidative stress, and epithelial injury. Current artificial tears mainly replenish aqueous volume and provide lubrication, but they may not adequately reproduce the coordinated interfacial functions of the native tear film that contribute to ocular surface stability. Here, we reported a tear film-inspired biomimetic strategy based on two complementary hyaluronic acid (HA) derivatives for the treatment of DED. HP was engineered by grafting zwitterionic poly(2-methacryloyloxyethyl phosphorylcholine) side chains onto HA to generate a highly hydrated, anti-evaporative, and low friction interface. Whereas HD was constructed by conjugating dopamine to HA to enhance ocular surface anchoring and provide intrinsic antioxidant activity. The integrated HP/HD system exhibited enhanced water retention, favorable shear-thinning behavior, and superior lubrication performance. Transverse relaxation ( T 2 ) NMR analysis further supported the key role of the zwitterionic hydration layer in interfacial lubrication. While quartz crystal microbalance with dissipation monitoring, fluorescence quenching, FTIR, in vitro and in vivo retention studies showed that HD strengthened mucin interaction and prolonged ocular surface residence. In addition, the catechol-containing component endowed the system with effective free radical scavenging capacity and intracellular reactive oxygen species suppression. In a benzalkonium chloride induced guinea pig model of DED, topical administration of HP/HD significantly improved tear secretion, accelerated corneal epithelial repair, promoted goblet cell recovery, and reduced corneal oxidative stress compared with the commercial lubricant control. Collectively, this work establishes a tear film-inspired biomimetic strategy that integrates anti-evaporation, hydration lubrication, surface anchoring, and antioxidation within a system, offering a promising material approach for DED therapy. Statement of Significance Dry eye disease (DED) causes severe discomfort and surface damage. Current treatments for DED primarily rely on transient aqueous supplementation, which inherently fails to reconstruct the hierarchical architecture of the native tear film and suffers from rapid precorneal clearance. To overcome this fundamental limitation, we proposed a tear film inspired Biomimetic Strategy. By integrating zwitterionic hydration lubrication (via PMPC-grafted hyaluronic acid) with catechol-mediated mucoadhesion and active antioxidant defense, our system synergistically reconstructs the physiological "mucin-aqueous-lipid" interface. Functionally, this system integrates functions such as anti-evaporation, moisturizing lubrication, surface anchoring and antioxidant protection, effectively breaking the vicious cycle of DED self-reinforcement. This work provides a physiologically informed biomaterial strategy that shifts the paradigm of DED management from passive moisture supplementation to Overall tear film reconstruction. Download: Download high-res image (263KB) Download: Download full-size image
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Small Methods
·
2026
·
IF 8.7
Xu Chen,Tianle Yang,Wenjie Zheng,Yingyi Luo,Ruixue Liang,Sanqi An,Xinli Liu
A Claringbullite-like nanozyme CuCl 0.38 F0.1(OH) 1.51 •nH 2 O (denoted as FCN) was fabricated by a simple “one-pot” method for non-small cell lung cancer (NSCLC) treatment. Acting as an “AND” logic gate, the pH/GSH dual-responsive property allowed FCN to selectively target tumor cells while minimizing side effects. FCN exhibited the glutathione catalase (CAT)-like, peroxidase (POD)-like, and peroxidase (GPx)-like activities. The enhanced catalytic activity of FCN was attributed to its improved charge transfer capability, as evidenced by its performance in H 2 O 2 decomposition. FCN prompted cuproptosis and ferroptosis by depriving glutathione (GSH), elevating ROS, alleviating hypoxia, and inhibiting glycolysis in A549 cells. Moreover, FCN elicited the active anti-tumor immune responses, including the macrophage phenotype transition, the elevated levels of CD8 + T cells, and the decreased levels of regulatory T (Treg) cells, thereby enhancing therapeutic efficacy against NSCLC. Furthermore, FCN treatment significantly attenuated lung metastasis in mice bearing Lewis lung carcinoma (LLC) cells. This work opens up a new avenue for the development of metal-halide nanozymes for tumor catalytic therapy.
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Nanomedicine-Nanotechnology Biology and Medicine
·
2026
·
IF 4.3
Guanghui Mei,Hanwen Wang,Xinhua Lin,Lingyi Huang
Triple-negative breast cancer (TNBC) remains a formidable challenge due to its aggressive progression and the absence of established therapeutic targets. This study engineered a multifunctional, tumor microenvironment (TME)-responsive nanoplatform MnO 2 @Man/DOX, which was designed for synergistic targeted chemotherapy and TME modulation. The platform comprises a manganese dioxide (MnO 2 ) core for redox regulation and a mannose (Man) shell for active targeting and metabolic sensitization, stabilized with bovine serum albumin and sodium dodecyl sulfate. MnO 2 @Man/DOX nanoparticles are nearly spherical (289 nm) and exhibit dual-responsiveness by efficiently depleting intracellular glutathione and catalyzing endogenous hydrogen peroxide into cytotoxic hydroxyl radicals via Fenton-like reactions. In vitro, the nanoplatform demonstrated a remarkable 8-fold reduction in IC 50 (0.52 μg/mL) compared with free doxorubicin (4.2 μg/mL) in 4T1 cells. Transcriptomic analysis suggested that MnO 2 @Man/DOX is associated with TNF signaling and apoptosis-related pathways, including extrinsic, intrinsic, and endoplasmic reticulum stress-mediated programs. In vivo evaluations in 4T1 tumor-bearing mice confirmed preferential tumor accumulation and superior growth inhibition with a high biosafety profile, including a hemolysis rate below 5% and minimal systemic toxicity. By integrating receptor-mediated targeting, redox homeostasis disruption, and chemosensitization, MnO 2 @Man/DOX offers a promising metabolism-oriented strategy for treating refractory TNBC.
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JOURNAL OF ELECTRONIC MATERIALS
·
2026
·
IF 2.8
Dai Han Yan,Xu Jing Wen,Zeng Han
In this work, we made a ternary composite made up of polydopamine-modified carbon nanotubes and Au nanoparticles that acts as a unit to hold a redox protein. The components within the ternary complex serve as a cofactor orientation guide, a conductive element, and an electron shuttle promoter, respectively. The electrochemical reactions occurring at this electrode were dominated by the redox process of the active cofactors in hemoglobin in coordination with polydopamine, achieving favorable efficiency with charge transfer of 69.8 s −1 . The hemoglobin-based electrode displayed an efficient electrocatalytic effect toward H 2 O 2 reduction with an onset potential of 0.058 V, close to the formal potential value for heme sites on hemoglobin. The normalized turnover frequency of the substrate in hemoglobin-induced electrocatalysis was estimated to be 7.0 × 10 2 s −1 . The as-prepared hemoglobin-based electrode exhibited favorable affinity, appropriate sensitivity, and a moderate detection limit toward the substrate ( K M = 0.214 mM, 1.01 × 10 −3 A·L·mol −1 , and 5.0 × 10 −3 mmol·L −1 ). The substrate diffusion process was identified as the key factor limiting the electrocatalytic performance of the hemoglobin-based electrode (2.23 × 10 −2 s −1 ). A glucose–H 2 O 2 biofuel cell was fabricated and could operate at an open-circuit potential of 0.72 V. Such a cell could produce a desirable power output density of ~5500 μW·cm −2 in the presence of a proton exchange membrane. Graphical Competitive ligation of heme protein with polydopamine could play a protective role against the negative effect of direct contact of the enzyme molecule with Au nanoparticles to retain the original configuration of native hemoglobin and exert its underlying electrocatalytic activity.
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Cell Death Discovery
·
2026
·
IF 10.4
Yuan Naonao,Ma Zhibo,Xue Zihan,Li Qingwen,Zhou Xi,Liu Jing,Lin Yanping,Gu Shiqi,Yi Sichuan,Lu Yao,Lan Peixiang
Distinct macrophage activation states play key roles in the formation and progression of heart allograft fibrosis. However, the exact molecular mechanisms that regulate the balance between inflammatory and pro-fibrotic macrophage responses during fibrosis remain poorly understood. Identifying and targeting the key molecule that regulates the differentiation of inflammatory and pro-fibrotic macrophages might be a pivotal strategy for mitigating fibrosis and prolonging allograft survival. Here, using single-cell sequencing analysis of human heart allografts fibrosis patient samples, we identified a population of macrophages that undergo epigenetic reprogramming through DNA methylation regulated by DNA methyltransferase DNMT1. DNMT1 small-molecule inhibitor 5-AzaC significantly attenuated graft fibrosis and prolonged allograft survival by inhibiting both inflammation and excessive tissue repair. Mechanistically, DNMT1-targeted macrophages suppress the DNA methylation level of the CpG island in the first intron of PTPRD, promoting PTPRD expression, which in turn inhibits the activity of STAT3 and STAT6 pathways, thereby suppressing the differentiation of inflammation and pro-fibrotic macrophages. Based on this, we developed a macrophage-targeted nanocarrier, MV/PEG-LPs, to load 5-AzaC, thereby enhancing its therapeutic precision for allograft fibrosis. Our results reveal a novel target, DNA methylation in macrophages, for the treatment of fibrosis-related diseases.
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