PHYTOMEDICINE
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2025
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IF 8.3
Yongyan Chen,Xu Han,Yuxuan Hao,Xu Wang,Fupeng Wu,Sheng Tan,Huijing Ye,Yang Hong,Xiaoyan Shen
Background Vascular calcification is a major cause of death in chronic kidney disease (CKD), with osteoblastic transdifferentiation of vascular smooth muscle cells (VSMCs) considered to be the crucial pathologic process. However, there remains a significant deficiency in effective prevention and treatment strategies. Purpose In an in vitro calcification screening model, we observed an inhibitory activity of Emodin on osteoblastic transdifferentiation of VSMCs. In the present study, we therefore aimed to evaluate its efficacy in CKD-induced medial vascular calcification in vitro and in vivo, and to further explore the underlying mechanisms. Study design A7R5 and MOVAS cells were treated with sodium phosphate to induce osteogenic transdifferentiation as in vitro models, while mice were fed with adenine and a high-phosphorus diet, and additionally received an intraperitoneal injection of 10,000 IU Vitamin D3 to induce chronic kidney disease (CKD) as an in vivo model. Vitamin K2 served as a positive control. Methods Alizarin Red S staining and VON-KOSSA staining were used to evaluate the effects of Emodin on osteogenic transdifferentiation. Western blotting, RT-qPCR and Von-Kossa staining were used to detect the effects of Emodin on aortic calcification in CKD mice in vivo. Chemical biology techniques including ITC, fluorescence titration, dual fluorescein reporter genes, CETSA, and DARTS, were used to detect the binding activity of Emodin to ERα and SYVN1. Immunoprecipitation, immunostaining, etc. were used to explore the mechanisms, and small molecule inhibitors and small RNA interference were used to verify the target of Emodin. Results Emodin could effectively inhibit the osteogenic transdifferentiation of A7R5 and MOVAS cells in vitro, and alleviate aortic calcification in CKD mice in vivo. Mechanism study revealed that Emodin could act as a molecular glue that binds directly to ERα and SYVN1 and enhances their interaction, thereby accelerating the ubiquitination degradation process of ERα. The decrease in ERα diminished the inhibition of ERα on the deacetylation of HIF-1α by SIRT6, thereby inhibiting VSMC osteogenic transdifferentiation and relieving the vascular cells calcification. Conclusion Our study demonstrates that ERα has a non-genomic effect to inhibit the deacetylation of HIF-1α by SIRT6, which can be abrogated by Emodin through SYVN1-mediated ERα degradation. These results provide evidences for Emodin to serve as a candidate drug for controlling clinical vascular calcification in CKD.
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Journal of Environmental Sciences
·
2026
·
IF 6.5
Caiyu Lian,Mingcheng Sun,Yue Li,Lin Wang
Cadmium (Cd) exposure triggers ferroptosis in renal tubular cells. • TFRC upregulation drives Cd‑induced ferroptosis by promoting iron influx. • HIF‑1α directly binds the TFRC promoter to transactivate its expression. • mPTP‑mediated calcium efflux activates CaMKII/HIF‑1α/TFRC axis. Cadmium (Cd) is a ubiquitous environmental pollutant and well-established nephrotoxicant primarily targeting renal proximal tubular cells. Ferroptosis, an iron‑dependent form of regulated cell death driven by lipid peroxidation, has recently emerged as a key mechanism in Cd‑induced kidney injury. Despite the central role of mitochondria in ferroptosis, the precise organellar events linking Cd exposure to ferroptotic execution remain obscure. Using Sprague‑Dawley rats and renal proximal tubular cells, we found that Cd exposure instigated ferroptosis, evidenced by iron overload, altered ferroptosis markers, lipid peroxidation, and typical mitochondrial morphology under transmission electron microscopy. Pharmacological inhibition of ferroptosis significantly attenuated Cd‑induced cellular damage, identifying ferroptosis as a critical driver. Mechanistically, Cd triggered opening of the mitochondrial permeability transition pore (mPTP), leading to mitochondrial calcium efflux and activation of calcium/calmodulin‑dependent protein kinase II (CaMKII). Activated CaMKII in turn increased hypoxia-inducible factor-1α (HIF-1α) transcription and promoted its nuclear accumulation. Notably, upregulated HIF‑1α directly bound to the promoter of transferrin receptor (TFRC) to stimulate expression of this key iron transport mediator, as confirmed by chromatin immunoprecipitation assay. Moreover, genetic knockdown of TFRC markedly attenuated Cd‑triggered ferroptosis and consequent cytotoxicity, establishing TFRC as a critical executioner of Cd‑evoked renal injury. Taken together, these findings delineate a novel signaling axis from mPTP‑mediated calcium efflux to HIF‑1α‑dependent TFRC transactivation that drives ferroptosis in Cd‑induced nephrotoxicity, offering a mechanistic basis for understanding and mitigating the renal health risks posed by environmental Cd exposure. Download: Download high-res image (405KB) Download: Download full-size image
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MATERIALS & DESIGN
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2026
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IF 8.2
Yue Peng,Cuiman Tang,Mingcong Niu,Tianyi Xu,QingYu Meng,Xinran Li,Rongheng Ma,Huimin Yu
A traditional medicine-inspired strategy provides a logical framework for constructing carrier-free hybrids. • Precise structural modifications successfully circumvent the inherent bioaccessibility limitations of natural products. • The covalent integration of diverse functional modules enables synergistic therapeutic efficacy against arthritis. • The therapeutic action is closely associated with the modulation of protein kinase B and hypoxia-inducible factor signaling. Curcumin (Cur) possesses potent anti-inflammatory activity but faces clinical challenges due to poor aqueous dispersibility, insufficient membrane affinity, and low bioavailability. Borneol (Bor), a classic “envoy” component in Traditional Chinese Medicine (TCM), exhibits prominent membrane-penetrating properties. Inspired by the “monarch-envoy” compatibility theory, we rationally designed carrier-free hybrids by covalently conjugating Cur (“monarch”) with Bor (“envoy”). Systematic characterization confirmed the successful synthesis and controllable optimization of key properties, including enhanced dispersibility, improved cellular uptake, and favorable biocompatibility. Using rheumatoid arthritis (RA) as a disease model, we identified SCBMS as the optimal formulation owing to its superior dispersibility and uptake, which directly translated into the most potent anti-RA efficacy. The hybrids exerted synergistic multifunctional effects—including robust anti-inflammatory and antioxidant activities—effectively reducing the arthritis index and ameliorating synovial hyperplasia and joint destruction in vivo . Mechanistically, our results indicate a close correlation between the therapeutic effects and the downregulation of the AKT/mTOR/HIF-1α signaling pathway, supporting the involvement of this pathway in the observed anti-RA activity. This study provides a generalizable framework for developing functional hybrids guided by TCM principles and validates their translational potential. Download: Download high-res image (152KB) Download: Download full-size image
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BIOCHEMICAL PHARMACOLOGY
·
2026
·
IF 6.5
Yating Liang,Xuehan Dou,Hao Huang,Yanfei Tang,Boqi Zhang,Wenhan Qiu,Jiabao Zheng,Yunzhang Liu,Yun Li,Junsheng Ye,Ling Lu
The cellular response to hypoxia is primarily orchestrated by the HIF (hypoxia-inducible factor) pathway, whose stability is regulated by PHD (prolyl hydroxylase domain) proteins. While PHD2 (prolyl hydroxylase domain-containing protein 2) serves as the principal regulator of HIF-α (hypoxia-inducible factor-α) stability and PHD1/3 (prolyl hydroxylase domain-containing protein 1/3) play subsidiary roles, the physiological function of P4HTM (prolyl 4-hydroxylase, transmembrane) remains poorly defined. Here, we demonstrate that p4htm knockout zebrafish exhibit constitutive Hif activation and develop systemic pathologies including erythrocytosis, pathological cardiac remodeling, and a novel HIF-dependent hepatic steatosis. Importantly, we establish that both pericardial edema and renal defects in p4htm mutants are mechanistically dependent on Hif signaling, as evidenced by rescue with Hif-α inhibition. Our findings identify p4htm as a key physiological regulator of Hif-mediated homeostasis in cardiovascular, renal, and metabolic systems.
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JOURNAL OF NANOBIOTECHNOLOGY
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2026
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IF 15
Wang Xuewei,Zhang Yue,Wu Hao,Yang Zelei,Ma Sufang,Li Lihong,Guo Lixia,Yan Lili,Zhang Boye,Liu Jianfei,Diao Haipeng,Ren Guodong,Zhang Chengwu,Liu Wen
Esophageal cancer (EC) is a highly malignant tumor that poses a significant threat to patient survival. Chemotherapy, a mainstay treatment for EC, often yields unsatisfactory outcomes due to chemotherapy resistance, the low efficacy of monotherapy and off-target toxicity. Therefore, it is imperative to develop one novel therapeutic strategy capable of overcoming drug resistance, enabling tumor microenvironment-responsive drug release, and achieving multimodal synergistic therapy. Currently, treatment of chemotherapy-resistant EC (CREC) faces great challenges. To address this, a pH-responsive nanoplatform, CDs-DOX-GOX@PEG (CDG@PEG), composed of iron-doped carbon dots (Fe-CDs), doxorubicin (DOX), glucose oxidase (GOX), and polyethylene glycol (PEG), was fabricated to improve CREC treatment through synergistic and targeted therapy. The physicochemical properties of CDG@PEG were characterized using TEM, XPS, XRD, FTIR and other techniques. Its anti-tumor efficacy was assessed with DOX-resistant KYSE-30 cells and corresponding xenograft mouse models. Moreover, the underlying therapeutic mechanism was further investigated via transcriptomic, immunofluorescence and immunohistochemical analyses. Physicochemical characterization results showed that the designed nanoplatform was successfully fabricated, which was endowed with outstanding pH-responsive behavior and O₂/ROS-generation capabilities. In vitro, CDG@PEG demonstrated excellent cellular uptake and potent tumor cell-killing capacities. In vivo, it displayed superior anti-tumor efficacy with good biocompatibility. Mechanistically, CDG@PEG realized the CREC therapy by down-regulating drug-resistant genes (such as HIF-1α related genes), inducing mitochondrial dysfunction, and triggering cell apoptosis. This work opened new avenues for developing novel therapeutic strategies against chemotherapy-resistant cancers. Graphical The alternative text for this image may have been generated using AI.
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EUROPEAN JOURNAL OF PHARMACOLOGY
·
2026
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IF 5.7
Jia Liu,Yangxian Chen,Mengyu Li,Guobao Chen,Junhui Yang,Ying Jiang,Xiao Zhang,Fang Li,Haibing Hua
Chronic atrophic gastritis (CAG) is a critical precancerous condition with limited therapeutic options to halt its progression toward gastric cancer. Targeting dysregulated metabolism and inflammation-driven transformation represents a promising yet underexplored strategy. Herein, through systematic screening of Jianwei Xiaoyan Granule (JWXYG)-derived compounds via molecular docking and surface plasmon resonance (SPR), we identified hederagenin as a potent and novel mechanistic target of rapamycin (mTOR) binder (Kd = 1.30 μM). In a rat CAG model, hederagenin administration resulted in marked histological and biochemical improvements. Histopathological evaluation revealed that hederagenin effectively restored gastric mucosal architecture, significantly attenuated characteristic glandular atrophy, and reduced the extent of intestinal metaplasia, a key precancerous lesion. Concurrently, serum analysis demonstrated that hederagenin treatment normalized critical biomarker levels, including a significant reduction in gastrin-17 (G-17) and the pro-inflammatory cytokine interleukin-6 (IL-6), alongside a notable increase in the levels of pepsinogen I (PG I) and pepsinogen II (PG II). Functionally, hederagenin exhibited potent anti-tumor properties in vitro by significantly suppressing the proliferation, migration, and invasion capabilities of premalignant gastric epithelial cells. Mechanistically, transcriptomic analyses revealed that hederagenin targeted cancer-associated metabolic reprogramming through the mTOR/hypoxia-inducible factor-1α (mTOR/HIF-1α) signaling axis. Experimental validation further confirmed that hederagenin significantly suppressed the mTOR/HIF-1α pathway. Additionally, it downregulated the expression of key rate-limiting glycolytic enzymes, including hexokinase II (HK II), pyruvate kinase M2 (PKM2), enolase 1 (ENO1), and lactate dehydrogenase A (LDHA), thereby attenuating glycolytic flux, a hallmark metabolic adaptation in precancerous lesions. Importantly, mTOR knockdown abolished hederagenin-mediated LDHA suppression and compromised its therapeutic efficacy, validating mTOR as an essential target. Our findings demonstrated that hederagenin could inhibit inflammation-cancer transformation in CAG via regulation of glycolysis through the mTOR/HIF-1α pathway, which provided new candidate compounds for regulating the transformation of CAG into cancer.
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PHYTOMEDICINE
·
2026
·
IF 11.3
Jing Chen,Gejing Li,Fang Zhao,Ye Zhang,Qingrui Mu,Junlan Zhang,Xiong Cai,Yuanyuan Tang
Background Cannabidiol (CBD), a major non-psychoactive phytocannabinoid derived from Cannabis sativa L., has shown therapeutic potential in rheumatoid arthritis (RA). However, the mechanisms by which CBD modulates synovial angiogenesis remain unclear. Purpose This study aimed to investigate whether CBD attenuates RA progression by suppressing synovial angiogenesis and to elucidate the underlying molecular mechanisms. Methods An adjuvant-induced arthritis (AIA) rat model was established to evaluate the therapeutic effects of CBD in vivo using arthritis scoring, micro-CT, and histopathological, immunohistochemical, and immunofluorescence analyses. In vitro , cytotoxicity was determined using the CCK-8 assay, followed by evaluations of CBD’s direct effects on the proliferation, migration, invasion, and inflammatory responses of RA fibroblast-like synoviocytes (RA-FLS) were evaluated, alongside Cell Counting Kit-8 (CCK-8) for cytotoxicity screening. Furthermore, the paracrine regulation of angiogenesis was assessed using a conditioned medium (CM) transfer system from hypoxia-stimulated RA-FLS applied to human umbilical vein endothelial cells (HUVECs). Molecular mechanisms were analyzed via Western blotting, RT-qPCR, ELISA, co-immunoprecipitation (Co-IP), molecular docking, and targeted proteasome inhibition (MG132). Results In vivo , CBD (5 and 10 mg/kg) treatment markedly alleviated joint inflammation, synovial angiogenesis, and structural bone destruction in AIA rats. In vitro , non-cytotoxic concentrations of CBD (2.4-4.8 μM) significantly suppressed aberrant RA-FLS proliferation, migration, invasion, and pro-inflammatory cytokine secretion. Mechanistically, CBD abrogated the hypoxia-induced accumulation of hypoxia-inducible factor-1α (HIF-1α) protein in RA-FLS without significantly altering HIF1A mRNA expression. This reduction was effectively reversed by MG132. Co-IP and molecular docking analyses revealed that CBD directly enhances the polyubiquitination of HIF-1α through stable structural interactions, driving a ubiquitin-proteasome-dependent degradation mechanism. Consequently, CBD dose-dependently decreased the extracellular secretion of vascular endothelial growth factor A (VEGFA) and angiopoietin-2 (ANG-2) from RA-FLS. Functionally, CM from CBD-treated RA-FLS disrupted the pro-angiogenic paracrine crosstalk—independent of direct CBD carryover—significantly impairing HUVEC migration, capillary-like tube formation, and downstream VEGFR2 (Tyr1175) phosphorylation. Conclusion CBD attenuates RA pathogenesis not only by directly suppressing RA-FLS hyperactivity but also by severing the pro-angiogenic paracrine crosstalk between RA-FLS and endothelial cells. These effects are driven by the ubiquitin-proteasome-dependent degradation of HIF-1α in RA-FLS via direct structural engagement, which depletes VEGFA/ANG-2 production and subsequent endothelial VEGFR2 activation. These findings highlight CBD as a promising disease-modifying anti-angiogenic therapeutic agent for RA. Download: Download high-res image (290KB) Download: Download full-size image
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PHYTOMEDICINE
·
2026
·
IF 11.3
Juan Zhan,JianHan Zhou,RunQiang Liu,ChaoChen Wu,YiHan Lai,Lin Jiang,Wei Wang,Meng Cheng,YiSen Shao
Objective : Tongue squamous cell carcinoma (TSCC) is characterized by high invasiveness and early lymph node metastasis, leading to a poor prognosis.Current surgical and chemoradiotherapy regimens often cause functional impairment, drug resistance, and other drawbacks. Thus, developing highly effective, low-toxicity treatments is a key research priority. Traditional Chinese medicine (TCM) offers unique advantages via multi-target synergistic effects, enabling innovative therapeutic approaches. Method : In this study, we developed Astragaloside IV-Brucea javanica oil nanoemulsion (AS/BJO-NEs) and characterized its stability, polydispersity, and pharmacokinetic profile. The effects of AS/BJO-NEs on TSCC cells were evaluated through a series of functional assays, including CCK-8 (viability), colony formation (proliferation), and scratch wound healing (migration). Both in vitro and in vivo experiments were performed to investigate whether its mechanism involves regulation of the MTFR2–HIF-1α–EZH2/FoxM1 signaling axis. Results The optimized AS/BJO-NEs exhibited uniform spherical morphology at the nanoscale and demonstrated favorable stability. In both in vitro and in vivo models, AS/BJO-NEs significantly suppressed the malignant phenotype of TSCC cells. Mechanistic investigation further revealed that the anti-tumor effects of AS/BJO-NEs are mediated, at least in part, through targeting the MTFR2–HIF-1α–EZH2/FoxM1 signaling axis, as confirmed by establishing stable MTFR2/HIF-1α knockdown and overexpression cell models. Conclusion : This study demonstrates that AS/BJO-NEs inhibit TSCC progression by targeting the MTFR2–HIF-1α–EZH2/FoxM1 signaling axis. Our findings provide experimental evidence supporting the development of multi-target therapeutic strategies derived from traditional Chinese medicine for the treatment of TSCC.
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MATERIALS & DESIGN
·
2026
·
IF 8.2
Hongbao Hou,Xu Li
Introduction Esophageal cancer (EC) is the most malignant tumor posing great threat to human health. Chemotherapy, as the first-line treatment for EC, can not yield expected outcome due to chemo-resistance, low efficacy of monotherapy and off-target toxicity. Hence, it is imperative to develop one novel therapeutic strategy that can realize anti-drug resistance, tumor microenvironment response drug release, and integrated multi-modal therapy. Objectives Currently, treatment of EC faces great challenges. One pH-responsive nanoplatform, CDs-DOX-GOx@PEG (CDG@PEG), composed of copper-doped carbon dots (Cu-CDs), doxorubicin (DOX), glucose oxidase (GOx), and polyethylene glycol (PEG), was fabricated to realize better treatment of EC via multi-modal synergistic and targeted therapy. Methods Microscopy. The physicochemical properties of CDG@PEG were determined via TEM, XPS, XRD, FTIR and so on. The anti-tumor capacity was assessed with KYSE-30 cells and xenograft mice models. Moreover, the therapeutic mechanism was assessed by transcriptome, immunofluorescence and immunohistochemical analysis. Results Physiochemical characterization results showed that as designed nanoplatform was successfully fabricated and was endowed with outstanding pH-responsive and O 2 /ROS-generation capacities. In vitro , CDG@PEG exhibited excellent cell uptake and potent tumor cell-killing effect. In vivo, CDG@PEG displayed superior anti-tumor effect accompanied by good biocompatibility. Mechanistically, CDG@PEG realized the EC therapy by down-regulating drug-resistant genes (such as HIF-1α related genes), inducing mitochondria dysfunction, triggering cell apoptosis. Conclusion One multifunctional nanoplatform, CDG@PEG, was successfully prepared and it exhibited excellent in vitro and in vivo anti-tumor effect, which open new venues for developing novel therapeutic strategies for chemo-resistance cancer.
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Biosensors-Basel
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2026
·Vol. 16
·期 5
·261
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IF 6.2
Ziyi Li,Yingxin Tian,Gefei Ren,Yingshu Guo
The overexpression of hypoxia-inducible factor-1α (HIF-1α) suppresses STING signaling and modulates lipid metabolism in tumor cells, leading to abnormal lipid droplet (LD) accumulation. Herein, we constructed a manganese dioxide (MnO2)-based nanomotor (HMIP@A). HMIP@A depletes intracellular hydrogen peroxide (H2O2) and glutathione (GSH) to generate oxygen (O2), reactive oxygen species (ROS), and manganese (Mn2+). A dual strategy of “oxygen supplementation” and “small-molecule inhibition” synergistically downregulates HIF-1α, thereby suppressing LD biogenesis. This process sensitizes tumor cells to ROS, leading to severe DNA damage. Released Mn2+and damaged DNA synergistically activate the cyclic GMP-AMP synthase (cGAS)-stimulator of interferon genes (STING) pathway. In vitro, HMIP@A markedly increases ROS production, lipid peroxidation (LPO), and DNA damage, thereby inducing tumor cell death, immunogenic cell death (ICD), and dendritic cell (DC) maturation. Furthermore, HMIP@A exhibits excellent penetration in tumor spheroids. Overall, this study provides a theoretical basis for the design of nanomedicines through a strategy integrating metabolic intervention, oxidative damage sensitization, and immune activation.
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ACS Nano
·
2025
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IF 16
Yan Fang,Feiyang Shen,Rui Huang,Yao Lin,Yijia Wu,Qian Li,Zhu Xie,Xiaoyu Yang,Zhe Zhang,Xiaoliang Jin,Xianqun Fan,Jianfeng Shen
The von Hippel–Lindau (VHL) tumor suppressor gene product, pVHL, is frequently deficient in a variety of human cancers. In addressing the treatment of pVHL-deficient tumors, hypoxia-inducible factor 2α (HIF-2α) has risen as a promising therapeutic target, culminating in the development of specific inhibitors like PT2385 and its analogues. Nonetheless, the absence of targeted delivery capabilities in these inhibitors heightens the risk of on-target toxicities. To mitigate these limitations, we have engineered a nanoparticle, termed PMMF (PT/MMSN@DSPE-PEG-FA), capable of delivering both a HIF-2α antagonist (PT2385) and manganese directly to tumor sites. PMMF has shown effective targeting of pVHL-deficient clear-cell renal cell carcinoma and melanoma, leading to significant therapeutic benefits and alleviating hypoxic and immunosuppressive traits of the tumor microenvironment. Functionally, PMMF boosts the cyclic GMP–AMP synthase–stimulator of interferon genes signaling pathway, which, in turn, stimulates a robust innate immune response. This response activates natural killer (NK) cells and CD8+ T lymphocytes while curbing the infiltration of regulatory T cells. Notably, the therapeutic efficacy of PMMF is markedly reduced when NK cells are blocked but not affected by neutrophil blockade, highlighting the critical role of NK cells in PMMF-induced antitumor immunity. Additionally, the safety profile of PMMF showed minimal systemic post-treatment cytotoxicity. In summary, our findings position PMMF as a promising platform for treating tumors with pVHL deficiency and underscore the therapeutic potential of metalloimmunotherapy.
研究领域:
肿瘤学
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免疫学
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纳米医学
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分子生物学
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NUTRITION AND CANCER-AN INTERNATIONAL JOURNAL
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2025
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IF 2.4
Jingjing Lu,Dongxuan Wang,Hongjin Huo,Hao Jiang,Wei Wei,Jie Sun,Fei Jiang
Triple-negative breast cancer (TNBC) is an aggressive subtype of breast cancer with high metastatic potential and limited therapeutic options. This study investigates the effects of calcitriol, an active metabolite of vitamin D, on TNBC progression by targeting the vitamin D receptor (VDR)-mediated hypoxia-inducible factor-1α (HIF-1α) axis. We established in vivo TNBC xenograft models using 4T1 cells and in vitro models with MDA-MB-231 and 4T1 cells overexpressing HIF-1α. Results showed that calcitriol inhibited lung metastasis and downregulated glycolytic activity in TNBC xenografts without affecting primary tumor growth. In vitro, calcitriol reduced cell viability, migration, and invasion by suppressing HIF-1α expression. It also decreased glucose uptake, lactate production, and ATP levels while downregulating key glycolytic regulators. VDR knockdown abolished these effects, confirming VDR as the critical mediator. Our findings suggest that calcitriol exerts anti-metastatic effects in TNBC by modulating the VDR-HIF-1α axis, inhibiting glycolysis, and suppressing the epithelial-mesenchymal transition. This study highlights the potential therapeutic role of calcitriol in TNBC treatment by targeting both metabolic reprogramming and invasive capacity. Future research should further explore the mechanisms underlying calcitriol-mediated HIF-1α suppression and its clinical application in TNBC.
研究领域:
肿瘤学
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分子生物学
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内分泌学
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癌症代谢
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转化医学
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