npj Clean Water
·
2025
·
IF 11.4
Jung Sung-Hyo,Hong Sung-Hak,Lee Youn-Jun,Park Seong-Jik,Jho Eun Hea,Lee Chang-Gu
Azo is a synthetic organic dye that has attracted considerable attention because of its recalcitrance to degradation and toxicity. An upgraded ozonation process must be developed that integrates decolorization, mineralization, and toxicity reduction to manage the residual azo dye in the effluent from the dyeing industry and reduce its associated aquatic environmental risks. In this study, an ozonation system using Meretrix lusoria (ML) shell-waste-derived biomass (ML800) that uses simple calcination was developed. The ML800/O 3 system almost completely decolorized ( > 99.0%) and highly mineralized (53.6 ± 1.7%) Congo red (CR) during (CR = 100 mg∙L –1 , ML800 = 0.5 g ∙ L –1 ), surpassing the performance of the other tested systems (single ozonation and single ML800). Moreover, the ML800/O 3 system reduced the acute toxicity of CR to the bacterium Aliivibrio fischeri , whereas single ozonation showed temporarily increased the toxicity of CR. The FE-SEM/EDS, FTIR, and XRD analyses verified that Ca(OH) 2 was the main calcium species in ML800, which catalyzed the decomposition of O 3 into highly reactive •OH. The system was successfully applied to various azo dyes and was robust with water matrix constituents. These findings highlight the potential of marine shell waste for use as a sustainable and ecofriendly additive for ozonation, increasing azo dye removal from wastewater in practical applications.
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IONICS
·
2025
·
IF 2.6
Wang Jing,Yao Chuan,Su Chang
The practical application of lithium metal batteries is hindered by the heterogeneous solid-electrolyte interphase (SEI), which undergoes repeated cracking and reconstruction during cycling, thereby exacerbating lithium dendrite growth. To address this issue, we propose an in-situ reconstruction strategy for the SEI layer by introducing the functional additive 1,3,5-trioxane (TO), which helps to homogenize lithium transport and enhance mechanical stability. By participating in the Li + solvation structure, TO facilitates the formation of a homogeneous and mechanically robust SEI, which preferentially promotes the formation of a polyoxymethylene (POM) phase and enriches LiF content within the SEI. This tailored interface significantly improves the uniformity of lithium deposition and interfacial compatibility. In coin cells employing a high-loading LiNi 0.90 Co 0.05 Mn 0.05 O 2 cathode (7.37 mg cm − 2 ) and an ultrathin lithium anode (50 μm), the TO-modified electrolyte enables a capacity retention of 73.1% after 200 cycles at 0.5 C, substantially outperforming the conventional electrolyte that retained only 25.9%. These results demonstrate the promising potential of this electrolyte design for high-energy-density lithium metal batteries.
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JOURNAL OF MATERIALS SCIENCE
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2025
·
IF 3.9
Gao Yang,Gao Shan,Zhang Yunhua,Lyu Shaoyi,Wang Feijun
Reuse of dye-containing wastewater for valuable products offers significant potential. Chitosan, a natural high-molecular-weight porous material, served as an effective carrier for dye molecules. This study uses chitosan to adsorb Congo Red, preparing hierarchical porous carbon materials, which are then applied in supercapacitors. The findings reveal that chitosan achieves an impressive adsorption capacity of 1450 mg g −1 for Congo Red. When the chitosan–Congo Red composite material-based carbon is used as the electrode material, it shows an outstanding specific capacitance of 318 F g −1 at a current density of 1 A g −1 . Furthermore, due to its high content of heteroatoms such as N, O, and S, the double-layer supercapacitor fabricated with this electrode material demonstrates a specific capacitance of 149.49 F g −1 at 1 A g −1 , with an energy density of 8.77 Wh kg −1 at a power density of 335.35 W kg −1 . These results highlight the considerable potential of this material after adsorption of dye-containing wastewater for applications in the energy storage field.
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Nature Communications
·
2025
·
IF 15.7
Bowen Liu,Yue Han,Yuan Jin,Meng Ye,Zeliang Yang,Jingyi Yang,Minglu Zhu,Xuyang Zhao,Yan Jin,Yuxin Yin
The quality control network in type 2 alveolar epithelial cells (AEC2s) is essential to respond to intrinsic and extrinsic challenges. However, the mechanisms that regulate AEC2 mitochondrial homeostasis remain unclear understood. Here, we report a role of G protein-coupled receptor class C group 5 member A (GPRC5A) in mitochondrial quality control in AEC2s through promoting mitochondrial secretion in extracellular vesicles (EVs). Utilizing mice models, we demonstrate that the disruption of GPRC5A specifically in AEC2s aggravates lung injuries. We further observe that GPRC5A deficiency in AEC2s reduces secretion of mitochondrial components in small-EVs and disrupts mitochondrial functions both in vitro and in vivo. Mechanistically, we determine that the GPRC5A-MIRO2 pathway facilitates the transfer of mitochondrial fragments into late endosomes. Collectively, our findings provide evidence of the shedding of mitochondrial components dependent on GPRC5A as a pathway of mitochondrial quality control in AEC2s, which is crucial in the maintenance of epithelial physiological activities and lung tissue homeostasis. The authors provide evidence of the secretion of mitochondrial components in extracellular vesicles dependent on GPRC5A as a pathway of mitochondrial quality control in AEC2s, which is essential for lung homeostasis maintenance.
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JOURNAL OF NANOBIOTECHNOLOGY
·
2025
·Vol. 24
·期 1
·103
·
IF 12.6
Zhang Yixun,Wang Xuehua,Zhang Hongli,Zhou Xin,He Huichan,Zou Fen,Zhuo Yangjia,Cai Zhouda,Xu Qianfeng,Xie Wenjie,Lin Jundong,Chen Muqi,Zheng Wenlian,Chen Jianwei,Liu Jinsheng,Yang Huikang,Zhong Weide,Yang Ronghua
Melanoma has a high incidence and mortality, and current therapies are limited. Here, we developed TCPC, an ER-targeted nanomedicine guided by omics analysis. It consists of curcumin-loaded PEG–PCL nanomicelles coated with a Tannic acid–Cu metal–polyphenol network. Guided by clinical transcriptome mining, we identified ER-stress vulnerabilities to inform material design. RNA-seq and imaging confirmed that TCPC preferentially accumulates in melanoma cells and localizes to the ER. TCPC markedly elevates CHOP expression, which triggers ER Ca²⁺ release, mitochondrial dysfunction, ROS accumulation, and apoptosis. Functionally, TCPC significantly suppresses cell viability, migration, and invasion in vitro. In melanoma xenografts, systemic TCPC treatment slows tumor growth, enhances intratumoral CHOP and Cleaved caspase-3, and induces apoptosis without systemic toxicity. Moreover, pharmacogenomic analyses revealed that CHOP upregulation correlates with increased sensitivity to several agents, and molecular docking highlighted Irinotecan and JQ1 as potential synergistic partners with TCPC. Collectively, this work demonstrates that nanomedicine guided by omics can couple organelle-specific delivery with ER-stress amplification to achieve potent antitumor efficacy. Overall, this work establishes an omics-guided materials strategy that integrates organelle-targeted delivery with ER-stress amplification for effective melanoma therapy. Graphical abstract
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Stem Cell Research & Therapy
·
2025
·
IF 7.3
Zhang Qinyao,Huang Shuwei,Liu Xiaoqian,Zhang Meijiu,Sun Jun,Liu Mingzhu,Nie Hemin,Lei Lei
Aim During the tooth-root elongation phase, dental epithelial stem cells (DESCs) cluster together and release various signaling molecules, facilitating the differentiation of stem cells from the apical papilla (SCAPs) into odontoblasts. This study aimed to investigate the regulatory mechanism of secretory proteins from DESCs cultured in a spherical system mimicking the in vivo microenvironment on the odontoblastic differentiation of SCAPs during root development, providing theoretical foundations and potential targets for dentin regeneration therapy based on epithelial-mesenchymal interactions. Methodology DESCs were isolated from the root tips of rodent incisors and cultured using low-attachment surface to mimic their in vivo clustering. The effects of spheroid culture (versus monolayer culture) on SCAPs viability and odontoblastic differentiation potential were systematically compared. Label-free mass spectrometry and bioinformatics analyses were employed to characterize the secretory protein profiles of DESCs under different culture conditions. In vitro and in vivo experiments validated the role of a key differential protein Lumican and its downstream signaling mechanisms. Results Compared to monolayer culture, spheroid culture significantly enhanced the secretion of Lumican by DESCs. Lumican demonstrated the ability to significantly promote dentin differentiation of SCAPs in vitro and in vivo. Mechanistic analysis revealed that Lumican binds specifically to integrin β1 (ITGβ1) on the SCAPs membrane, thereby activating the downstream ERK signaling pathway to mediate its pro-differentiation effects. Conclusion This study illustrates that spheroid culture can restore the epithelial microenvironment of DESCs, leading to the release of Lumican, which targets SCAPs. This research uncovers the crucial roles of Lumican and ITGβ1 in DESCs-SACPs interactions and paves the way for potential therapeutic strategies in dentin regeneration. Graphical abstract
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高影响因子
CATALYSIS LETTERS
·
2025
·Vol. 156
·期 1
·21
·
IF 2.4
Yang Jihui,Shi Minghao,Zheng Jiahao,Zhang Shule,Zhong Qin
Ammonia Selective Catalytic Reduction (NH₃-SCR) is highly effective for nitrogen oxide (NO x ) removal, yet its low-temperature activity remains a key limitation for broader applications. We developed an innovative series of microporous N, O-codoped carbon catalysts (NOAC-x) that facilitate the fast SCR reaction. Results demonstrate that the synergy between catalyst micropore structure and surface functional groups governs denitrification performance: Low-temperature calcination induces pore blockage by nitrogen-containing groups (pyridinic N), reducing specific surface area and weakening NH₃/NO adsorption capacity.Moderate calcinatio promotes partial decomposition of nitrogen groups, optimizing the micropore structure while preserving active sites such as carboxyl groups and pyridinic N, thereby significantly enhancing catalytic activity.High-temperature calcinatio triggers pore collapse and decomposition of active groups, degrading performance.NOAC-600 achieved 95% NO x conversion at 120 °C and exhibited merely a 2% activity decline during a 108-hour stability test. This work provides theoretical guidance for designing microporous N, O-dual-doped carbon-based catalysts and underscores the critical importance of micropore structure and surface chemistry optimization in low-temperature SCR technology. Graphical
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INFLAMMATION
·
2018
·Vol. 41
·期 4
·1384-1395
·
IF 2.884
Su Yang,Lu Jingxiao,Chen Xianguo,Liang Chaozhao,Luo Pengcheng,Qin Cong,Zhang Jie
Chronic prostatitis (CP) is a clinically common disease with high morbidity. It affects the patients’ quality of life (QoL) as well as physical and mental health seriously due to the recurring symptoms of lower urinary tract and genitalia. As the opinions about the etiology of CP are still not uniform, it is very difficult to be treated or even cured. Autophagy is a highly conserved physiological function which is widely found in eukaryotic cells. In general, cells maintain a certain level of autophagy under physiological conditions, and the basal level of autophagy can be regulated by a variety of autophagy-related genes under stress such as hunger, infection, trauma, and other circumstances. Therefore, the main purpose of this study is to investigate the role of autophagy in chronic nonbacterial prostatitis (CNP, also called CP). In this paper, we established the CNP model via hypodermic injection of 17β-estradiol and subsequently abdominal rapamycin (a common autophagy inducer) treatment based on castrated rats. Then, the expression of nuclear factor-κB (NF-κB), interleukin-1β (IL-1β), and autophagy-related markers as well as autophagosome formation in prostate tissues, peripheral blood mononuclear cells (PBMCs), and serum of rats were evaluated respectively. In addition to some histological changes in the prostate tissues, we found the levels of NF-κB and IL-1β were significantly increased in the model group, along with significantly suppressed autophagy, whereas rapamycin could reverse these effects which involved in the mTOR/ULK1/ATG13 signaling pathway. In conclusion, our results suggested that rapamycin could ameliorate hormone imbalance-induced CNP by activating autophagy.
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Cancer Cell International
·
2021
·Vol. 21
·期 1
·1-15
·
IF 5.722
Lv Minchao,Xu Qingxin,Zhang Bei,Yang Zhiqiang,Xie Jun,Guo Jinku,He Feixiong,Wang Wei
Background Osteosarcoma is the third most common cancer in adolescence and the first common primary malignant tumor of bone. The long-term prognosis of osteosarcoma still remains unsatisfactory in the past decades. Therefore, development of novel therapeutic agents which are effective to osteosarcoma and are safe to normal tissue simultaneously is quite essential and urgent. Methods Firstly, MTT assay, cell colony formation assay, cell migration and invasion assays were conducted to evaluate the inhibitory effects of imperatorin towards human osteosarcoma cells. RNA-sequence assay and bioinformatic analysis were then performed to filtrate and assume the potential imperatorin-induced cell death route and signaling pathway. Moreover, quantitative real-time PCR assay, western blot assay and rescue experiments were conducted to confirm the assumptions of bioinformatic analysis. Finally, a subcutaneous tumor-transplanted nude mouse model was established and applied to evaluate the internal effect of imperatorin on osteosarcoma by HE and immunohistochemistry staining. Results Imperatorin triggered time-dependent and dose-dependent inhibition of tumor growth mainly by inducing autophagy promotion and G0/G1 phase arrest in vitro and in vivo. Besides, imperatorin treatment elevated the expression level of PTEN and p21, down-regulated the phosphorylation of AKT and mTOR. In contrast, the inhibition of PTEN using Bpv (HOpic), a potential and selective inhibitor of PTEN, concurrently rescued imperatorin-induced autophagy promotion, cell cycle arrest and inactivation of PTEN-PI3K-AKT-mTOR/p21 pathway. Conclusions This work firstly revealed that imperatorin induced autophagy and cell cycle arrest through PTEN-PI3K-AKT-mTOR/p21 signaling pathway by targeting and up-regulating PTEN in human osteosarcoma cells. Hence, imperatorin is a desirable candidate for clinical treatments of osteosarcoma.
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高影响因子
INFLAMMATION RESEARCH
·
2014
·Vol. 63
·期 7
·597-608
·
IF 2.143
Pan Xiaolong,Cao Xiang,Li Na,Xu Yimiao,Wu Qiuyue,Bai Jing,Yin Zhimin,Luo Lan,Lan Lei
Objective Forsythin (FOR) is an active ingredient extracted from the fruit of the medicinal plant Forsythia suspensa (Thunb.) Vahl. Here, we investigated the effect of FOR on LPS-induced inflammatory response and the underlying molecular mechanisms in RAW264.7 macrophages. Materials and methods RAW264.7 cells were pre-treated with or without FOR and then stimulated with or without LPS. The productions of TNF-α, IL-1β, IL-6, PGE 2 and NO were determined by ELISA and nitrite analysis, respectively. The expressions of nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) were measured by Western blotting and RT-PCR analysis. The activations of signaling molecules were detected by Western blotting using phosphorylation specific antibodies. Reactive oxygen species (ROS) production was determined by ROS assay. Results LPS-induced productions of IL-1β, IL-6, TNF-α, NO and PGE 2 were inhibited by FOR in a dose-dependent manner. FOR also suppressed the LPS-elevated expressions of iNOS and COX-2. Further investigations revealed that FOR significantly inhibited the LPS-induced activations of JAK-STATs and p38 MAPKs, but not of IKKα/β in LPS-stimulated RAW264.7 cells. Additionally, FOR interfered with both JAK-STATs and p38 MAPKs signaling pathways to modulate the expressions of IL-1β, IL-6, TNF-α, iNOS and COX-2. Furthermore, FOR reduced the LPS-induced ROS accumulation, validating that FOR serves as an antioxidant. Conclusions Our data suggested that FOR exerts anti-inflammatory action, at least in part, via suppressing LPS-induced activation of JAK-STATs and p38 MAPKs signalings and production of ROS in macrophage cells.
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Cell and Bioscience
·
2021
·Vol. 11
·期 1
·1-16
·
IF 7.133
Xu Hongfei,Wang Zhen,Chen Miao,Zhao Wenting,Tao Tingting,Ma Liang,Ni Yiming,Li Weidong
Background Pathological cardiac hypertrophy is a major contributor of heart failure (HF), which seriously threatens human’s health world widely. Deregulation of m6A RNA methylation, and m6A methyltransferases and de-methyltransferases have been demonstrated to act essential roles in cardiac hypertrophy and HF. Here, we studied the potential roles and its underlying mechanisms of m6A Reader YTHDF proteins in HF. In this study, we constructed HF mouse model by transverse aortic constriction surgery. Primary cardiomyocytes were isolated and stimulated with isoproterenol (ISO) or phenylephrine (PHE) to induce myocardial hypertrophy.Results Through single-cell RNA-seq analysis, immunofluorescent staining, HE staining, Western blotting, and real time-PCR detections, we found that YTHDF2 mRNA and protein level, but not YTHDF1 or YTHDF3, was significantly increased during HF development. YTHDF2 overexpression could efficiently alleviate cardiac hypertrophy. Furthermore, through immunoprecipitation accompanied with mass spectrometry analysis, Gene Ontology (GO) analysis, and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis, we found that ISO stimulation did not evidently affect YTHDF2-interacting proteins. However, ISO or PHE stimulation significantly increased YTHDF2 protein interacting with Myh7 (beta-myosin heavy chain) mRNA, an important cardiac hypertrophy marker, in an m6A-dependent manner. Knockdown of Myh7 or deletion of the YTH domain of YTHDF2 reversed the protective effects of YTHDF2 on cardiac hypertrophy. Finally, we found that ISO or PHE stimulation promoted YTHDF2 protein expression through enhancing Ythdf2 mRNA stability in an m6A-dependent manner in cardiomyocytes.Conclusion sOverall, our results indicate that the m6A Reader YTHDF2 suppresses cardiac hypertrophy via Myh7 mRNA decoy in an m6A-dependent manner. This study highlights the functional importance of YTHDF2-dependent cardiac m6A mRNA regulation during cardiac hypertrophy, and provides a novel mechanistic insight into the therapeutic mechanisms of YTHDF2.
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Cell Death & Disease
·
2018
·Vol. 9
·期 6
·1-14
·
IF 5.638
Tao Liang,Lin Hongfa,Wen Jingjing,Sun Qi,Gao Yan,Xu Xi,Wang Junsong,Zhang Jianfa,Weng Dan
Endoplasmic reticulum (ER) stress contributes to the development and progression of many chronic inflammatory diseases, including type 2 diabetes, obesity, atherosclerosis, neurodegenerative diseases, and cancer. ER stress has been reported to induce inflammasome activation and release of mature IL-1β, which contributes to many inflammatory diseases. The molecular mechanisms that activate the inflammasome during ER stress are still poorly understood. Here we report that the kinase receptor-interacting protein 1 (RIP1) plays an important role in ER stress-induced activation of inflammasome. Inhibition of RIP1 kinase activity by Necrostatin-1 or siRNA-mediated RIP1 knockdown significantly reduced ER stress-induced caspase-1 cleavage and IL-1β secretion in both bone marrow-derived macrophages (BMDMs) and J774A.1 macrophages. We speculate that the mitochondria fission factor dynamin-related protein 1 (DRP1) and reactive oxygen species (ROS) might function as the effectors downstream of RIP1 to mediate inflammasome activation. Our study reveals a critical role for RIP1 in regulating ER stress-induced inflammation responses, and proposes RIP1 as a potential pharmaceutical target to treat diseases resulting from unresolved ER stress-related inflammation.
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