Nature Communications
·
2026
·
IF 18.1
Yu Hongwei,Xin Xing,Ge Jiawen,Luo Yunyun,Cui Yanming,Zang Xu-Feng,Xu Tonghui,Zheng Tianle,Mandic Zoran,Xia Yongyao,Zhou Mingjiong
Lithium metal batteries offer a pathway toward next-generation energy storage due to their high specific energy. However, their implementation remains challenging, particularly under lean electrolyte conditions, where unstable interfaces and inefficient ion transport severely limit cycling stability. Here, we show a bifunctional ligand-bridged electrolyte by integrating ethyl difluoroacetate into a lithium nitrate/triethyl phosphate matrix. Incorporating ethyl difluoroacetate as a dynamic bridging agent drives the formation of interconnected ionic aggregates through synergistic H δ+ − O δ− hydrogen bonding with anions and coordination interactions with Li⁺, thereby accelerating interfacial kinetics and suppressing parasitic reactions. The electrolyte further enables weakly coordinating solvents to engage in the solvation sheath via non-classical hydrogen bonding, facilitating the formation of a robust, inorganic-rich solid electrolyte interphase. This design enables the realization of high-capacity (14 Ah) Li ‖ Ni95 pouch cells, which achieve a specific energy of 606.8 Wh kg −1 while maintaining 92.9% capacity retention after 75 cycles at rates of 0.1 C/0.2 C. These findings demonstrate a viable electrolyte strategy for enabling high-performance lithium metal batteries under practical conditions.
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ACS Nano
·
2026
·
IF 17.3
Guangyu Ma,Yuting Li,Xiang Li,Dehong Yu,Minghao Chao,Jiale Li,Jintao Guo,Ke Wang,Zhao Liu,Rongrong Sun,Fenglei Gao
Intracellular ion homeostasis is essential for cellular function; tumor cells remodel ion networks to sustain malignant proliferation. Targeting ion homeostasis represents a promising anticancer strategy. Cuproptosis and ferroptosis, emerging programmed cell death modalities, exploit tumor-specific ionic vulnerabilities but are constrained by mechanisms including ATPase copper transporter (ATP7A)-mediated Cu2+ efflux and the solute carrier family 7, member 11 (SLC7A11/xCT)-driven antioxidant axis. We developed an ion-mediated immunotherapeutic nanoplatform (CCZSM) that disrupts Cu2+ and Fe2+ metabolism while activating antitumor immunity. Zn2+ enhances zinc transporter 1 (ZNT1) expression to increase Cu2+ influx; concurrent ATP7A silencing inhibits Cu2+ efflux, inducing cuproptosis. Mitochondrial Fe2+ release combined with Co2+-induced free Fe2+ generates an “Fe2+ storm” that, alongside Cu2+-mediated disruption of cysteine (Cys) metabolism, compromises antioxidant defenses and triggers ferroptosis. This ionic dysregulation induces tumor cell death and promotes release of damage-associated molecular patterns (DAMPs) and mitochondrial DNA (mtDNA), activating immunogenic cell death (ICD) and the cGAS-STING pathway. Resultant dendritic cell (DC) maturation and T-cell activation link ion metabolic interference to systemic immune responses. This study establishes a multi-ion metabolic intervention strategy, advancing tumor immunotherapy paradigms.
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JOURNAL OF CATALYSIS
·
2026
·
IF 6
Zeyu Wang,Huijuan Shao,Ai Zhang,Ying Zhang,Chen Luo,Tao Jiang,Yating Wang
Porous organic polymers (POPs) are promising heterogeneous catalyst supports. However, their application in ethylene tetramerization for high-value 1-octene (1-C 8 ) is limited by nonuniform metal coordination and poorly controlled pore-confined reactions. Here, one-step solvent thermal polymerization was carried out by vinyl functionalized full diphosphine (PNP) ligand to synthesize POPs derived from the PNP ligand and used as a support for chromium-based catalysts. The characterization confirms that the interaction between POPs, modified methylaluminoxane (MMAO) and Cr(III) chloride tetrahydrofuran complex promotes the formation of Cr(III) active sites, and the chemical coordination environment of the support determines the concentration of these Cr(III) species. The adjustable POPs framework can selectively produce linear alpha-olefins (C 4 , C 6 and C 8 ) with different carbon numbers. Notably, POP-2, which exhibited a larger pore size, lower steric hindrance and a higher density of Cr(III) active sites, showed exceptional catalytic performance in the ethylene tetramerization reaction under 1 MPa and 45℃ conditions, achieving 51.54% of C 8 selectivity (1-C 8 accounted for 97.6%), C 6 /C 8 total selectivity of 88.11%, and high catalytic activity of 8.08 × 10 5 g(mol·Cr) −1 h −1 . Whereas the high-steric-hindrance POP-3 system is predisposed to trimerization. The calculation of density functional theory (DFT) revealed that the tetramerization pathway is energetically preferred over the trimerization pathway in the POPs/Cr(III) system. These results further clarified that product carbon number distribution is dually governed by the Gibbs free energy barriers of trimerization/tetramerization and the steric hindrance of Cr(III) active centers. Collectively, these findings highlight the remarkable application potential of POPs as tunable matrices for engineering Cr(III) sites and fabricating high-selectivity ethylene oligomerization catalysts.
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CHEMICO-BIOLOGICAL INTERACTIONS
·
2026
·
IF 5.2
Lubin Xie,Chuhang Chi,Chengshuang Pan,Nianci Chen,Yunbing Tang,Shaowei Wang,Ren-shan Ge,Qianjin Fei
Halogenated disinfectants are widely used in medical, household, and industrial settings, but their inhibitory effects on 17β-hydroxysteroid dehydrogenase 1 (17β-HSD1), a key enzyme catalyzing estrone-to-estradiol (E 2 ) conversion, remain unclear. We evaluated nine compounds for inhibition of human placental and rat ovarian 17β-HSD1 using enzymatic assays, kinetic analysis, BeWo cell E 2 production assays, 3D quantitative structure-activity relationship (3D-QSAR), molecular docking, molecular dynamics simulations (MDS), absorption, distribution, metabolism, excretion, and toxicity (ADMET) prediction, and network toxicology. Six compounds inhibited human 17β-HSD1, with half-maximal inhibitory concentration (IC 50 ) values of 0.78-14.90 μM; potency followed hexachlorophene > bithionol > bromochlorophene > fenticlor > dichlorophene > chlorophene. Rat 17β-HSD1 was inhibited by these six compounds and by triclosan, with IC 50 values of 6.13-54.77 μM. Kinetic analysis indicated mainly mixed/noncompetitive inhibition. In BeWo cells, fenticlor decreased E 2 production at ≥ 1 μM, dichlorophene at 10 and 20 μM, and bromochlorophene and hexachlorophene at 20 μM, whereas chlorophene and bithionol were inactive up to 20 μM. The 3D-QSAR model and descriptor analysis suggested associations of inhibition with hydrophobicity, aromatic features, molecular size and halogenation. Docking and 100-ns MDS supported stable binding of active compounds near the nicotinamide adenine dinucleotide phosphate (NADPH)-binding region, particularly for hexachlorophene. Network toxicology placed HSD17B1, which encodes 17β-HSD1, within preeclampsia-related estrogen and steroidogenic pathways. These findings indicate that halogenated disinfectants may disrupt estrogen homeostasis through direct 17β-HSD1 inhibition and warrant further evaluation for reproductive and placental endocrine toxicity.
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JOURNAL OF AGRICULTURAL AND FOOD CHEMISTRY
·
2025
·
IF 6.2
Weikang Sun,Renjie Luo,Qingwei Qu,Jie Yang,Guang Yang,Lihua Song,Peng Cao,Erguang Li
Plant-based phenolic components and their metabolites, such as ellagic acid (EA) and urolithin A (UA), possess a variety of biological activities. Here, we investigated the antiviral effect of EA and UA against HSV-1 infection, a virus that causes peripheral infection as well as brain inflammation. Both compounds demonstrated potent antiviral activity. Network pharmacology and molecular docking analyses identified protein kinase CK2 as a common target for their action. We showed that both EA and UA were direct CK2 inhibitors using an enzymatic assay, an observation substantiated in cell culture studies. The effect of EA and UA on HSV-1 infection through CK2 was confirmed in CK2 (CSNK2B) knockout cells. Finally, we demonstrated an antiviral effect using a murine model of herpetic stromal keratitis. EA or UA treatment reduced HSV-1 shedding and prevented viral neuroinvasion. CK2 is a critical enzyme involved in cell proliferation and the proinflammatory response. In addition to identifying CK2 as a putative target of EA and UA antiviral activities, this study also demonstrates that EA and its metabolite UA have the potential to reduce infection-associated neurodegenerative inflammation.
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POLYMER
·
2025
·
IF 4.5
Guangshui Tu,Chong Wang,Shengyou Chen,Qian Wang,Zhenxue Liu,Haotian Zhou,Chunyu Feng,Handou Zheng,Haiyang Gao
Heterogeneous catalysts have long dominated polyolefin production, the immobilization of a pyridylamido hafnium catalyst is highly challenging because of its unique in-situ ligand modification mechanism. Here, we report a heterogeneous pyridylamido hafnium catalyst immobilized on a dual MgCl 2 /Al i Bu n (2-ethyl-1-hexoxide) 3-n activator/support for slurry homo- and copolymerization of 4-methyl-1-pentene (4MP). The supported pyridylamido hafnium catalyst shows enhanced catalytic activity and excellent polymer morphology control toward homopolymerization of 4-methyl-1-pentene. The produced poly(4-methyl-1-pentene)s show high isotacticity (>99%) and high melting temperatures up to 230 °C, and have normal molecular weight distribution. The heterogeneous catalyst still remains the advantages of enhanced catalytic activity and excellent polymer morphology control during the copolymerization of 4MP and α-olefins. Both the incorporation of α-olefin and longer chain α-olefins can improve the resilience of PMP materials.
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CRYSTENGCOMM
·
2024
·Vol. 26
·期 38
·5469-5478
·
IF 2.6
Shengjie Zhu,Xiaomin Zhang,Lei Dong,Yangyang Yuan,Xiuyun Ma,Yanping Chen,Lei Xu
Hierarchically structured materials are considered to be one of the important options to enhance the mass transportation efficiency in microporous zeolites. Herein, we reported a highly efficient steam-assisted crystallization strategy for the synthesis of a hierarchical TS-1 zeolite with a tunable macropore size. The amorphous SiO2–TiO2 precursor dissolved gradually and acted as both a nutrient supplier and macropore template in situ. The framework Ti content of the synthesized TS-1 zeolites could be tuned over a wide range (Ti wt% = 0.70–1.39) by varying the Ti content of the SiO2–TiO2 precursor. Moreover, the pore size of the macropores could be modulated according to the particle size of the precursor based on the investigation of the formation mechanism of the macropores in the hierarchical TS-1 zeolite. The hierarchical TS-1 zeolite exhibited better catalytic activity in the epoxidation reaction of 1-hexene and hydroxylation of phenol compared to the typical microporous zeolites. The improved performance of the hierarchical TS-1 zeolite was probably caused by the improved diffusion performance of the hierarchical structure.
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PHARMACOLOGICAL RESEARCH
·
2022
·
IF 10.334
Xingda Li,Yang Zhang,Yue Zhao,Yang Zhou,Qilong Han,Ying Yang,Lingmin Zhang,Ling Shi,Xuexin Jin,Ruixin Zhang,Haiyu Gao,Genlong Xue,Desheng Li,Zhi-Ren Zhang,Yanjie Lu,Baofeng Yang,Zhenwei Pan
Pathological cardiac hypertrophy is a process characterized by significant disturbance of protein turnover. Cullin-associated and Neddylation-dissociated 1 (CAND1) acts as a coordinator to modulate substrate protein degradation by promoting the formation of specific cullin-based ubiquitin ligase 3 complex in response to substrate accumulation, which thereby facilitate the maintaining of normal protein homeostasis. Accumulation of calcineurin is critical in the pathogenesis of cardiac hypertrophy and heart failure. However, whether CAND1 titrates the degradation of hypertrophy related protein eg. calcineurin and regulates cardiac hypertrophy remains unknown. Therefore, we aim to explore the role of CAND1 in cardiac hypertrophy and heart failure and the underlying molecular mechanism. Here, we found that the protein level of CAND1 was increased in cardiac tissues from heart failure (HF) patients and TAC mice, whereas the mRNA level did not change. CAND1-KO+ /- aggravated TAC-induced cardiac hypertrophic phenotypes; in contrast, CAND1-Tg attenuated the maladaptive cardiac remodeling . At the molecular level, CAND1 overexpression downregulated, whereas CAND1-KO+ /- or knockdown upregulated calcineurin expression at both in vivo and in vitro conditions. Mechanistically, CAND1 overexpression favored the assembly of Cul1/atrogin1/calcineurin complex and rendered the ubiquitination and degradation of calcineurin. Notably, CAND1 deficiency-induced hypertrophic phenotypes were partially rescued by knockdown of calcineurin, and application of exogenous CAND1 prevented TAC-induced cardiac hypertrophy. Taken together, our findings demonstrate that CAND1 exerts a protective effect against cardiac hypertrophy and heart failure partially by inducing the degradation of calcineurin.
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NEUROCHEMISTRY INTERNATIONAL
·
2026
·
IF 5.5
Zhipeng Lu,Yang Long,Xiang Li,Le Zhang,Jie Bai
The clinical utility of morphine is limited by the development of tolerance and addiction. These processes are linked to neuroinflammation involved microglial responses. Thioredoxin-1 (Trx-1) is a crucial endogenous antioxidant with neuroprotective properties, and our previous work has shown that Trx-1 overexpression blocks morphine-induced conditioned place preference (CPP). However, the role of Trx-1 in morphine-induced microglial inflammatory responses remains unclear. Here, we investigated the effects and underlying mechanisms of Trx-1 overexpression on morphine-induced microglial pro-inflammatory shifts, both in the microglial cell line BV-2 and in the ventral tegmental area (VTA) of mice. In vitro, morphine treatment increased intracellular reactive oxygen species (ROS) in BV-2 cells, upregulated markers associated with microglial reactivity (IBA-1 and MHC-II), activated the NF-κB pathway (evidenced by increased p -IκBα and nuclear p65 translocation), and elevated pro-inflammatory cytokines (IL-1β, IL-6, TNF-α) while reducing the anti-inflammatory cytokine IL-10. Overexpression of Trx-1 via adenoviral transduction reversed all these morphine-induced effects. In vivo, using a CPP paradigm, we confirmed that morphine CPP was blocked in Trx-1 transgenic (TG) mice. Biochemical analysis of the VTA from these mice revealed that Trx-1 overexpression similarly attenuated morphine-induced upregulation of IBA-1, MHC-II, and pro-inflammatory cytokines, consistent with in vitro results. Mechanistically, co-immunoprecipitation assays demonstrated an endogenous interaction between Trx-1 and the mu-opioid receptor (MOR). Overexpression of Trx-1 significantly enhanced this interaction and was associated with increased MOR expression. These results reveal that overexpression of Trx-1 suppresses morphine-induced neuroinflammation by binding MOR and reducing ROS-driven NF-κB activation in microglia. This mechanism positions Trx-1 as a potential therapeutic target for improving the clinical safety and efficacy of opioid addiction.
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FOOD RESEARCH INTERNATIONAL
·
2026
·
IF 8.8
Ronggang Jiang,Hongyu Chen,Jian Ouyang,Hao Xu,Kuofei Wang,Xingchang Ou,Yun Peng,Jinhua Chen,Zhonghua Liu,Jianan Huang
Baojing Huangjincha 1 green tea (HJC) is characterized by a fresh floral aroma with a distinctive milky note, setting it apart from both conventional and other novel green tea varieties. However, the key odorants contributing to this unique profile have not yet been fully identified. In this study, 109 common volatile compounds were detected from 22 HJC samples using comprehensive two-dimensional gas chromatography coupled with quadrupole time-of-flight mass spectrometry (GC × GC-QTOFMS). Headspace solid-phase microextraction combined with gas chromatography-olfactometry (HS-SPME-GC-O) and aroma extract dilution analysis (AEDA) were employed to identify 28 aroma-active compounds (FD ≥ 8), 18 (OAV ≥ 1) of which were quantified in the tea infusion. The accuracy of these results was validated by an aroma recombination model that closely replicated the original aromatic profile of HJC. Omission and addition experiments further revealed six critical odorants as pivotal contributors to the overall aroma, including geraniol, linalool, heptanal, 2-methylbutyraldehyde, hexanal, and phenylethyl alcohol. Moreover, molecular docking analysis indicated that phenethyl alcohol, linalool, and geraniol form stable conformations with olfactory receptors OR1A1 and OR5M3, facilitated by van der Waals forces, hydrogen bonds, and hydrophobic interactions. These findings provide a foundational theoretical framework for optimizing green tea processing techniques and enhancing quality control standards.
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MICROCHIMICA ACTA
·
2026
·Vol. 193
·期 5
·321
·
IF 5.4
Liu Shicong,Zhang Yuanyuan,Zhao Hongyang,Liu Junqiu,Hou Chunxi
A “turn-on” fluorescence sensor was developed for cholesterol detection on the basis of fluorescence resonance energy transfer (FRET) between the organic fluorophore 1-(4-(1,2,2-triphenylvinyl)phenyl)pyrene (TPE-Py) and a gold nanoparticle-β-cyclodextrin conjugate (AuNPs-β-CD). Mechanistically, the AuNPs-β-CD, an energy acceptor, was synthesized via Au–S bonding, and TPE-Py transferred energy to the AuNPs via FRET, resulting in fluorescence quenching of TPE-Py. In the presence of cholesterol, which has a stronger binding affinity for the β-CD cavity, TPE-Py was competitively displaced, enabling the recovery of the fluorescence signal. This sensor has high sensitivity for cholesterol, with a low detection limit of 66 nM and a linear range of 0.5–30 µM. Furthermore, the sensor was successfully used to determine the cholesterol content in food samples with satisfactory recoveries, revealing its potential for food analysis.
Section
Graphical abstract
The alternative text for this image may have been generated using AI.
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Cancer Communications
·
2026
·
IF 28.4
Chenchen Hu,Feiming Hu,Changjian Shao,Yuanli He,Liping Su,Daimei Shi,Lingying Yu,Yuanjie Sun,Jing Wang,Xiyang Zhang,Hongtao Duan,Junqi Zhang,Yubo Sun,Dongbo Jiang,Xiaolong Yan,Shuya Yang,Kun Yang
Background: Lung cancer remains a major global health burden. RNA-binding proteins (RBPs) play crucial roles in post-transcriptional gene regulation, and their dysregulation is frequently implicated in tumorigenesis. The present study aimed to elucidate the molecular network governed by the highly expressed RBP TIMELESS in lung adenocarcinoma (LUAD) and determine its mechanistic role in LUAD progression. Methods: The Cancer Genome Atlas-LUAD, Gene Expression Omnibus, and single-cell RNA sequencing datasets were analyzed to identify aberrantly expressed RBP genes. The RBP gene TIMELESS exhibited the most significant effect on LUAD cell death and was selected for further study. Photoactivatable ribonucleoside-enhanced crosslinking and immunoprecipitation sequencing and RNA sequencing were employed to identify ferroptosis-related targets directly bound by TIMELESS. Molecular mechanisms underlying the TIMELESS-mediated regulation of ferroptosis in LUAD were investigated via immunoprecipitation–mass spectrometry, glutathione S -transferase pull-down, immunofluorescence–fluorescence in situ hybridization, RNA immunoprecipitation, poly(A)-tail, and RNA stability assays. In an orthotopic lung cancer mouse model treated with erastin (a ferroptosis inducer) and programmed cell death protein 1 (PD-1) blockade, the role of TIMELESS in therapeutic response was assessed via flow cytometry and multiplex immunofluorescence (mIF). Infiltrating immune cells in LUAD were analyzed by tissue microarrays (TMAs) via mIF. Results: TIMELESS significantly affected LUAD cell proliferation and death, and TIMELESS knockdown significantly enriched RNA-binding and ferroptosis pathways. Transferrin (TF) was identified as a direct TIMELESS target governing ferroptosis. TIMELESS was revealed to bind Ccr4-Not transcription complex subunit 3 (CNOT3) to promote TF mRNA degradation. TIMELESS depletion combined with erastin and PD-1 blockade enhances efficacy, prolongs survival, increases T cell and M1 macrophage infiltration, and reduces M2 macrophage infiltration. Further, high TIMELESS expression was inversely correlated with ferroptosis marker 4-hydroxynonenal but positively correlated with programmed cell death ligand 1 (PD-L1), reduced T cell and M1 macrophage infiltration, and increased M2 macrophage infiltration. Conclusions: TIMELESS recruits CNOT3 to accelerate TF mRNA degradation, thereby suppressing ferroptosis and promoting LUAD growth. These findings suggest that the TIMELESS/TF regulatory axis may be a promising therapeutic target for LUAD.
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