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Journal of Water Process Engineering · 2026 · IF 6.7

Construction of WO3/ZnIn2S4 Z-scheme heterojunction by electrostatic self-assembly to enhance charge separation and reactive oxygen species generation

Mengge Yan,Tingting Liu,Yushan Hu,Wenlong Bai,Mingfei Wei,Yuxuan Zhang,Xusheng He,Ru Li

This study successfully fabricated a WO 3 /ZnIn 2 S 4 (WO 3 /ZIS) composite photocatalyst via electrostatic self-assembly under acidic conditions (pH = 4.1). The effect of composite ratio on the material's structure and optoelectronic properties was systematically investigated using multiple characterization techniques, including XRD, SEM, TEM, BET, UV–Vis spectroscopy, and electrochemical measurements. Photocatalytic mechanism studies were conducted using fluvastatin as a model pharmaceutical pollutant. Results confirm the formation of a Z-scheme heterojunction in the WO 3 /ZIS composite. Increasing the proportion of ZnIn 2 S 4 during electrostatic self-assembly effectively enlarges the specific surface area, enhances visible-light absorption, and suppresses the recombination of photogenerated e − -h + pairs, thereby significantly improving photocatalytic performance. The WO 3 /ZIS-30 % composite material exhibited the most stable structure, the largest specific surface area, and the optimal light absorption capacity and charge carrier separation efficiency. Its degradation efficiency for fluvastatin reached 59.81 %, representing a 25.88 % improvement over WO 3 . Radical trapping experiments verify the simultaneous generation of ·OH and ·O 2 − radicals, and the concentrations of ·O 2 − and ·OH were 1.68 × 10 −5  mol/L and 1.61 × 10 −5  mol/Land their synergistic action considerably strengthens the oxidative power of the system. The Z-scheme heterojunction formed by electrostatic self-assembly facilitates spatial separation of photo generated charges and enables multi-radical oxidation, collectively boosting photocatalytic efficiency. This work provides a new strategy for designing highly efficient and stable photocatalysts suited for removing pharmaceutical contaminants from water.

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mBio · 2022 ·Vol. 14 ·期 1 · IF 7.786

A Small Molecule Inhibitor of Erg251 Makes Fluconazole Fungicidal by Inhibiting the Synthesis of the 14α-Methylsterols

Hui Lu,Wanqian Li,Malcolm Whiteway,Hongkang Wang,Shuo Zhu,Zhe Ji,Yanru Feng,Lan Yan,Ting Fang,Liping Li,Tingjunhong Ni,Xiaolong Zhang,Quanzhen Lv,Zichao Ding,Lijuan Qiu,Dazhi Zhang,Yuanying Jiang

Fluconazole (FLC) is widely used to prevent and treat invasive fungal infections. However, FLC is a fungistatic agent, allowing clinical FLC-susceptible isolates to tolerate FLC. Making FLC fungicidal in combination with adjuvants is a promising strategy to avoid FLC resistance and eliminate the persistence and recurrence of fungal infections. Here, we identify a new small molecule compound, CZ66, that can make FLC fungicidal. The mechanism of action of CZ66 is targeting the C-4 sterol methyl oxidase, encoded by the ERG251 gene, resulting in decreased content of sterols with the 14α-methyl group and ultimately eliminating FLC tolerance of Candida albicans. CZ66 most likely interacts with Erg251 through residues Glu195, Gly206, and Arg241. Establishing Erg251 as a synergistic lethal target protein of FLC should direct research to identify specific small molecule inhibitors of 14α-methylsterol synthesis and open the way to abolishing fungal FLC tolerance.IMPORTANCE Fluconazole (FLC) tolerance increases the frequency of acquired FLC resistance, and a high FLC tolerance level is associated with persistent candidemia. Multiple functional proteins, such as calcineurin, heat shock protein 90 (Hsp90), and ADP ribosylation factor, are essential for the survival of C. albicans exposed to FLC, but how these factors increase the fungicidal activity of FLC remains to be determined. In this study, we found that 14α-methylsterols replace ergosterol to allow C. albicans to survive FLC, but Erg251 inactivated by CZ66 results in loss of 14α-methylsterol synthesis and cell death of C. albicans treated with FLC. Establishing Erg251 as a synergistic lethal target protein of FLC should direct research to identify specific small molecule inhibitors of 14α-methylsterol synthesis and open the way to abolishing fungal FLC tolerance.

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ACS Nano · 2022 · IF 18.027

Inhalable Biomimetic Protein Corona-Mediated Nanoreactor for Self-Amplified Lung Adenocarcinoma Ferroptosis Therapy

Wenhao Wang,Fangqin Fu,Zhengwei Huang,Wenhua Wang,Minglong Chen,Xiao Yue,Jintao Fu,Xiaoqian Feng,Ying Huang,Chuanbin Wu,Xin Pan

Ferroptosis therapy by catalyzing the Fenton reaction has emerged as a promising tumor elimination strategy for lung adenocarcinoma (ADC). However, the unsatisfactory Fenton reaction efficiency, strong intracellular antioxidant system, and insufficient lung drug accumulation limits the ferroptosis therapeutic effect. To address these issues, an inhalable nanoreactor was proposed by spontaneously adsorbing biomimetic protein corona (PC) composed of matrix metalloproteinase 2 responsive gelatin and glutamate (Glu) on the surface of cationic nanostructured lipid carriers (NLC) core loaded with ferrocene (Fc) and fluvastatin. The prepared Fc-NLC(F)@PC could be nebulized into lung lesions with 2.6 times higher drug accumulation and boost lipid peroxide production by 3.2 times to enhance ferroptosis therapy. Mechanically, fluvastatin was proved to inhibit monocarboxylic acid transporter 4 mediated lactate efflux, inducing tumor acidosis to boost Fc-catalyzing reactive oxygen species production, while the extracellular elevating Glu concentration was found to inhibit xCT (system Xc–) functions and further collapse the tumor antioxidant system by glutathione synthesis suppression. Mitochondrial dysfunction and cell membrane damage were involved in the nanoreactor-driven ferroptotic cell death process. The enhanced antitumor effects by combination of tumor acidosis and antioxidant system collapse were confirmed in an orthotopic lung ADC tumor model. Overall, the proposed nanoreactor highlights the pulmonary delivery approach for local lung ADC treatment and underscores the great potential of ferroptosis therapy.

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ADVANCED MATERIALS · 2025 · IF 26.8

Bioinspired Liquid Pockets with Externally Induced Internal Microscale Flow

Lian Xu,Feng Wu,Yigang Shen,Yi Fan,Shuli Wang,Xu Hou

The gastric mucosal barrier, through its gastric pits, serves as a pathway for secretions, ensuring that mucus produced by the gastric glands is transferred to the gastric lumen, providing stable protection. Here a bioinspired liquid pockets material is shown, composed of a thermo-driven hydrogel that acts as an external activation unit to release interflowing liquid responsively, and porous matrices that serve as interconnected pockets to transfer it, enabling controlled internal flow and adaptive barrier functionality. Experiments and theoretical analysis demonstrate the stability and regulatory mechanisms of these liquid pockets, based on the interconnected pockets between the external activation unit and internal fluid flow. It exhibits a new pathway for regulating microscale flow at responsive material interfaces, enabling applications from sequential drug release, self-cleaning, and antifouling to anti-swelling. These unique capabilities address long-standing challenges in microscale flow control, with potential impacts in diverse fields including microfluidics, drug delivery, medical devices, 3D printing, and beyond.

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BIOCHEMICAL PHARMACOLOGY · 2025 · IF 5.6

Pitavastatin overcomes multi-drug resistance in CRC and NSCLC by targeting the NRP1-ZFX axis

Yuan-yuan Zhai,Qiang Wang,Qi-yao Nong,Mei-yu Gao,Ying Zhang,Qin-wen Xiao,Yuan Tian,Zun-jian Zhang,Feng-guo Xu,Pei Zhang

Multidrug resistance (MDR) is a significant challenge in cancer treatment, with limited effective strategies available. Neuropilin-1 (NRP1) is emerging as a potential therapeutic target for overcoming drug resistance, but its role in MDR and the identification of potential inhibitors require further exploration. In this study, we investigated the role of NRP1 in MDR and identifies potential inhibitors targeting NRP1. Elevated NRP1 expression was observed in oxaliplatin (OXP)-resistant HCT116 (HCT116/L) and cisplatin (DDP)-resistant A549 cells (A549/DDP). Virtual screening and biological assays identified pitavastatin (Ptv) as a potent NRP1 inhibitor that restored chemosensitivity in resistant cells both in vitro and in vivo . Mechanistic studies revealed that Ptv directly binds to NRP1, promotes degradation of Zinc finger X-chromosomal protein (ZFX), and disrupts the NRP1-ZFX axis to reverse MDR. This study provides promising prospects for targeting the NRP1-ZFX axis as a therapeutic strategy for MDR and highlights the potential clinical application of Ptv in diseases involving NRP1.

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