Journal of Radiation Research and Applied Sciences
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2025
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IF 2.5
Yu Zhang,Hongbo Lv,Chao Chen,Zixu Li,Zhaoyu Xie,Miaomiao Wu,Zhixu Zhu,Ying Fan,Jing Li,Qiang Gao,Jun Han,Hui Che,Lan Ma
Background Ischemic stroke (IS) is a major global cause of mortality and long-term disability, and effective therapies are urgently needed. Hydrogen sulfide (H 2 S) has shown neuroprotective effects in various neurological disorders, but its mechanisms in IS remain unclear. This study aims to explore the role and mechanism of H 2 S in IS treatment. Methods IS models were established in vivo using middle-cerebral-artery occlusion (MCAO) in rats and in vitro using oxygen-glucose deprivation/reoxygenation (OGD/R) in PC12 cells. These models were treated with H 2 S donors NaHS or GYY4137. Pathological features were evaluated using TTC, FJC, H&E, and Nissl staining. Cell viability was assessed with live/dead staining and CCK-8 assay. RNA sequencing identified gene expression changes after H 2 S treatment under OGD/R conditions. Ferroptosis-related markers, lipid peroxidation (GSH, SOD, MDA), ROS levels, and the expression of SLC7A11 and GPX4 were measured by flow cytometry, Western blot, and immunofluorescence. MiR-27a levels were quantified by qRT-PCR. Results NaHS administration in MCAO rats reduced infarct volume, increased Nissl body density, and decreased degenerating neurons. GYY4137 exhibited similar neuroprotective effects in vitro. RNA sequencing revealed that GYY4137 reversed ferroptosis-related gene changes, including SLC7A11. H 2 S supplementation inhibited neuronal ferroptosis, shown by increased SLC7A11 and GPX4 expression, elevated GSH and SOD levels, and reduced MDA content. Additionally, MCAO or OGD/R induced miR-27a expression, which negatively regulated SLC7A11. H 2 S reversed this induction, and miR-27a overexpression partially blocked the anti-ferroptotic effect of H 2 S. Conclusion H 2 S alleviated IS-induced brain injury by suppressing ferroptosis, partially through miR-27a-dependent regulation of SLC7A11. These findings suggest H 2 S as a promising therapeutic agent for IS, warranting further clinical exploration.
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ACS Applied Nano Materials
·
2025
·
IF 5.5
Shu-jing Hong,Chao Qin,Zi-fan You,Ye-lei Zhang,Kang Wang,Xiao Jia,Wen-ge Liu
Ferroptosis is a reactive oxygen species (ROS)-dependent cell death pathway. The synergistic integration of multimodal ROS-based therapies, such as photodynamic therapy (PDT) and chemodynamic therapy (CDT), to amplify lipid peroxidation represents a potential approach for enhancing ferroptosis-mediated antitumor effects. However, the tumor microenvironment (TME), where insufficient endogenous substrates (e.g., H2O2, O2) and elevated antioxidant defenses (e.g., glutathione, GSH), undermines the efficacy of most ROS-based therapies, thereby limiting ferroptosis-driven tumor eradication. To address this challenge, we developed a multifunctional nanoreactor ZnO2@ZnPc@Fe3+-tannic acid that orchestrates a ferroptosis-inducing cascade through self-sustained H2O2 supply, GSH depletion-mediated TME modulation, and combined PDT/CDT with mitochondrial dysfunction induction. Under the acidic and GSH-rich TME, the metal-phenolic network shell of ZPFT degraded, releasing Fe3+ that was subsequently reduced to Fe2+. Meanwhile, the exposed ZnO2 decomposed to generate H2O2, which fueled Fe2+-mediated Fenton reactions to produce abundant •OH radicals. These radicals synergize with 1O2 generated by ZnPc to collectively trigger a ROS storm. Concurrently, ZnO2-derived Zn2+ induced intracellular zinc overload, which cooperated with PDT/CDT to exacerbate mitochondrial dysfunction, and consequently disrupt the tumor’s antioxidant defenses. This cascade led to significant downregulation of key ferroptosis markers, GPX4 and SLC7A11. This study developed a therapeutic strategy against drug-resistant tumors by remodeling the TME limitations to simultaneously induce a ROS storm and dismantle antioxidant barriers, achieving highly efficient ferroptosis activation.
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Research
·
2025
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IF 10.7
Chengjunyu Zhang,Sen Liu,Jianhui Zhang,Junlin Lu,Zehua Chen,Bolin Pan,Chu Liu,Ming Huang,Hengji Zhan,Hongjin Wang,Siting Chen,Kaiwen Jie,Baoqing He,Jingdie Wu,Ye Li,Haifeng Wang,Jing Zhao,Qiang Zhang,Xu Chen
Ferroptosis has promising potential for augmenting antitumor effects, but monotherapy with ferroptosis inducers in vivo has been reported to have limited efficacy in tumor management. The development of synergistic strategies with targeted capabilities is crucial for enhancing the antitumor efficacy of ferroptosis inducers. In this study, we designed and characterized a novel self-assembled nanomedicine by mixing ferrous ions (Fe 2+ ) and epigallocatechin gallate (EGCG) in a controllable manner and encapsulating the ferroptosis inducer RSL3, named Fe-EGCG@RSL3. This multifunctional nanomedicine effectively induces ferroptosis and growth inhibition in bladder cancer cells and patient-derived organoids. In vivo, Fe-EGCG@RSL3 was enriched in the subcutaneous tumors of allogenic and xenograft mouse models, thereby substantially overcoming RSL3 resistance. Intravesical instillation of Fe-EGCG@RSL3 controls orthotopic bladder tumor progression. Furthermore, nanomedicine potentiates the therapeutic effect of anti-programmed cell death protein 1 (PD1) immunotherapy by increasing the cytotoxicity of CD8 + T cells to cancer cells and modulating the proportions of both T-cell and myeloid cell subpopulations within the tumor immune microenvironment. Overall, Fe-EGCG@RSL3 has dual functions as a multifaceted nanomedicine that integrates ferroptosis induction with immunomodulation, offering a novel and clinically translatable strategy for bladder cancer therapy.
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ECOTOXICOLOGY AND ENVIRONMENTAL SAFETY
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2026
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IF 6.6
Xiao Liang,Qi Huang,Yang Wu,Deyu Zhu,Zhuangzhuang Wei,Qing Feng,Zhilong Chen,Yibing Chen,Ping Ma,Xu Yang,Cuiyu Bao,Xinyu Bao
Background Polystyrene microplastics (PS-MPs) represent a major environmental contaminant, capable of building up in various organisms, including animals and plants. They can increase through the food chain, ultimately threatening human health. Recent research has indicated a possible association between exposure to PS-MPs in the environment and heart damage; nevertheless, the specific mechanisms behind this connection are not yet fully understood. Objectives This study aimed to investigate the toxic effects of PS-MPs exposure on cardiac health. We specifically elucidated the underlying mechanisms through which PS-MPs exacerbate doxorubicin hydrochloride (DOX)-induced cardiac injury, emphasizing oxidative stress, ferroptosis, and dysregulation of mitochondrial dynamics. Furthermore, we examined the protective effects of two antagonists: Ferrostatin-1 (Fer-1) and luteolin (Lut), against PS-MPs-induced cardiac injury. Methods C57BL/6 mice were categorized into eight distinct groups: the blank control group (saline), the PS-MPs exposure group (PS-MPs), the DOX modeling group (DOX), the combined exposure group of PS-MPs and DOX (PS-MPs+DOX), and the treatment groups with Fer-1 and Lut (PS-MPs+Fer-1, PS-MPs+Lut, PS-MPs+DOX+Fer-1, PS-MPs+DOX+Lut). The entire experimental duration spanned five weeks. We evaluated the effects of PS-MPs and DOX on cardiac function using electrocardiography and assessed their impact on cardiac injury through histopathological analysis of the heart. Concurrently, we examined the effects of PS-MPs and DOX on mitochondrial structure via mitochondrial electron microscopy. Furthermore, we analyzed the heart organ coefficient, myocardial injury markers (CK-MB, CTnT), oxidative stress biomarkers (ROS, MDA, GSH, 4-HNE, Nrf2), ferroptosis-related markers (Fe 2 + , GPX4, SLC7A11), mitochondrial damage markers (ATP, Complex III, Complex V), mitochondrial dynamics-related markers (OPA1, MNF2, DRP1), as well as serum metabolomics. Results Our findings reveal that exposure to PS-MPs exhibits significant cardiotoxic effects, influencing heart rate changes in mice and leading to abnormal in oxidative stress levels and ferroptosis-related proteins within myocardial tissue. Concurrently, exposure to PS-MPs leads to changes in mitochondrial structure and dynamics, further exacerbating oxidative stress and ferroptosis. Ultimately, PS-MPs aggravate DOX-induced cardiac injury. However, Fer-1 and Lut have a good improvement effect on the above situation. Furthermore, metabolomic analyses suggest that pathways and metabolites involved in cAMP signaling, the TCA cycle, tryptophan metabolism, and the metabolism of xenobiotics by cytochrome P450 may also play significant roles. Conclusion PS-MPs exposure can further exacerbate DOX-induced cardiac injury in mice, a process characterized by oxidative damage, activation of the ferroptosis pathway, and alterations in mitochondrial dynamics. Furthermore, luteolin, a naturally occurring active compound, plays a significant role in ameliorating this process.
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JOURNAL OF ETHNOPHARMACOLOGY
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2026
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IF 6.8
Zhengwang Guo,Huifeng Hao,Xinxin Deng,Yanna Jiao,Bin Dong,Dong Xue,Shu-Yan Han
Ethnopharmacological relevance Triple-negative breast cancer (TNBC) has a poor clinical prognosis and shows resistance to traditional treatments. Ferroptosis is a potential therapeutic strategy for TNBC. Although dandelion extract has demonstrated anti-tumor effects against TNBC, its role in regulating ferroptosis has not been elucidated. Aim of the study This study aimed to investigate the role and mechanisms of dandelion extract in inhibiting TNBC via the induction of ferroptosis. Materials and methods Cell viability and cell death were detected by CCK-8 assay and PI/Hoechst 33342 dual staining, respectively. Proteomic profiling was used to identify the mechanisms of dandelion extract-induced cell death. Ferroptosis was assessed by measuring key hallmarks, including Fe 2+ accumulation, lipid peroxidation, mitochondrial dysfunction, and ultrastructural changes. Mechanistic validation was achieved through target-specific interference and subsequent biomolecular analysis. Results Dandelion extract selectively induced cell death in TNBC cells without affecting normal MCF-10A cells. Proteomic and experimental evidence indicates that dandelion extract induces ferroptosis in TNBC cells, characterized by elevated Fe 2+ , ROS, lipid peroxidation, MDA levels, and mitochondrial dysfunction. Crucially, ferroptosis inhibitors attenuated the inhibitory effect of dandelion extract on TNBC cell viability, confirming ferroptosis as the primary cell death mechanism. Mechanistic studies have demonstrated that dandelion extract promoted ferroptosis in TNBC cells both in vitro and in vivo through NCOA4-mediated ferritinophagy. Conclusions This study demonstrates that dandelion extract induces ferroptosis in TNBC cells both in vitro and i n vivo by regulating ferritinophagy mediated by the NCOA4-FTH1 axis, thus suggesting novel therapeutic strategies for TNBC treatment.
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Journal of Ginseng Research
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2026
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IF 5.6
Hongbo Zhu,Hang Li,Yinong Shi,Jinhui Liu,Hua Zhi,Xuelu Zhao,Zhiwen Wang,Fumin Ping
Background Pressure injuries (PIs) remain a therapeutic challenge due to persistent inflammation and ferroptosis-driven tissue damage. Ginsenoside Rb1, a key bioactive component of Panax ginseng, demonstrates anti-inflammatory and anti-ferroptotic properties, but its clinical application is limited by poor bioavailability and rapid degradation in wound environments. Purpose This study aimed to develop a chitosan/alginate nanocomposite hydrogel loaded with ginsenoside Rb1 (Rb1@CS@ALG) to enhance Rb1 delivery and investigate its therapeutic mechanisms in PI repair, focusing on SIRT1-AMPK-mediated ferroptosis inhibition and angiogenesis promotion. Methods The pH-responsive Rb1@CS@ALG hydrogel was synthesized and characterized (TEM/DLS/HPLC). In vitro studies evaluated ferroptosis markers (GPX4, SLC7A11), ROS levels, and cell migration in HaCaT cells under ischemia-reperfusion. A rat PI model (n=6/group) assessed wound closure rates, histopathology (H&E/Masson's), and protein expression (CD31/Col I). RNA-seq analyzed differential gene expression. Results The hydrogel showed sustained Rb1 release (82.3% at 24 h) and pH-dependent drug delivery. Treatment upregulated GPX4/SLC7A11 (2.3-fold) while reducing ROS (58%) and ACSL4 (45%) via SIRT1-AMPK activation (p-AMPK↑2.9-fold). In vivo, it accelerated wound closure by 75% (vs. controls, p<0.001), increased angiogenesis (CD31↑3.1-fold), and improved collagen organization (Col I/III ratio↑2.7-fold). RNA-seq confirmed enrichment in ferroptosis and extracellular matrix pathways. Conclusion This study establishes ginsenoside Rb1 as a potent therapeutic agent for PIs when delivered via nanocomposite hydrogel, with dual mechanisms of ferroptosis inhibition and angiogenesis activation. The findings provide a scientific foundation for applying ginseng-derived compounds in chronic wound management.
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ACS Omega
·
2026
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IF 4.3
Xianghuai Zheng,Yue Zou,Qinkai Xie,Hao Dong,Jiating Lin,Xianxian Zhuang,Ruoting Xian,Shaobing Li
Oral squamous cell carcinoma (OSCC) presents significant therapeutic challenges due to chemoresistance and limited treatment modalities. Black phosphorus nanosheets (BPNSs), a novel two-dimensional nanomaterial, have shown promising antitumor effects. However, their role in inducing ferroptosis in OSCC and the underlying mechanisms remain to be elucidated. In this study, BPNSs were prepared via liquid-phase exfoliation, and their effects on the OSCC CAL-27 cells were subsequently evaluated. In vitro, BPNSs dose-dependently inhibited CAL-27 cell proliferation, induced G2/M phase arrest, and triggered ferroptosis, indicated by increased intracellular Fe2+, ROS, and lipid peroxidation, along with decreased glutathione (GSH) levels and altered expression of ferroptosis-related proteins (ACSL4, NCOA4, and GPX4). These effects were attenuated by ferroptosis inhibitor ferrostatin-1. In vivo, BPNSs suppressed CAL-27 xenograft growth without systemic toxicity, with elevated tumor malondialdehyde (MDA) and Fe2+ confirming ferroptosis. Mechanistic studies indicated that BPNSs inhibited the PI3K-AKT pathway, leading to the downregulation of SREBP1. Overexpression of SREBP1 attenuated BPNS-induced ferroptosis, confirming its critical role. These findings suggest that BPNSs induce ferroptosis in OSCC via the PI3K-AKT-SREBP1 signaling pathway, providing a novel therapeutic strategy for OSCC treatment.
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AQUACULTURE
·
2026
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IF 3.9
Yi-Ran Zhao,Tong-Hao Wang,Ze-Xin Zhao,Xiao-Tian Niu,Hong-Ming Lv,Yan-Bing Li,Yang Cao,Mu-Yang Li
In the present study, we evaluated the effects of deoxynivalenol (DON) on intestinal oxidative stress, immunity, ferroptosis, and endoplasmic reticulum stress in Channa argus . Furthermore, we investigated the mechanism underlying DON-induced cytotoxicity by inhibiting ACSL4 in macrophages. In vivo analysis demonstrated DON inhibits growth and even leading to increased mortality. DON induces intestinal ROS and iron ion accumulation, thereby causing endoplasmic reticulum dysfunction and triggering oxidative stress and ferroptosis. This process is accompanied by decreased levels of ferroptosis-inhibiting proteins (GPX4, FPN1, and FSP1), along with increased ACSL4 and ROS levels. Furthermore, DON-induced ROS accumulation elicits endoplasmic reticulum dysfunction and drives the progression of immunosuppression and inflammation. In vitro analysis demonstrated that inhibition of ACSL4 affects macrophage activity as well as ROS and ATP levels, representing a potential intervention strategy to restore immune cell function. This study demonstrates that targeting ACSL4 may serve as a potential strategy for alleviating DON-mediated intestinal injury in C. argus .
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International Journal of Nanomedicine
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2026
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IF 6.5
Dezhao Chen,Xiaohan Zheng,Qiao Gao,Bing Chen,Yang Sun
Purpose: Natural ferritin Fn) is a cage-like protein with a central cavity, making it a promising vehicle for drug delivery. However, its non-specific accumulation in iron-metabolizing organs impairs targeting precision and therapeutic efficacy. To overcome this challenge, we aimed to develop a novel biomimetic nanoplatform based on manganese-mineralized ferritin loaded with dihydroartemisinin (DHA@MFn) for precise ovarian cancer treatment, enabling controlled drug release and amplified therapeutic effects within the tumor microenvironment.Methods: We constructed a manganese-mineralized ferritin nanocage encapsulating DHA, resulting in DHA@MFn with favorable physicochemical properties, including a particle size of 12.2 nm and a zeta potential of − 13.54 mV. The stability, stimuli-responsiveness, and in vitro release behavior of DHA@MFn were evaluated under weakly acidic conditions. We assessed its ability to catalyze Fenton-like reactions releasing Mn2+, induce ferroptosis via lipid peroxidation and GSH depletion, and enable controlled drug release. In vivo biodistribution, tumor accumulation, and therapeutic efficacy were investigated using SKOV3 tumor-bearing mice, alone and in combination with irradiation.Results: DHA@MFn remained stable and demonstrated excellent responsiveness to the tumor microenvironment, releasing Mn2+ ions that catalyzed Fenton-like reactions for hydroxyl radical production. The nanoplatform facilitated targeted tumor accumulation and retention, significantly reducing off-target organ distribution, particularly in the liver. The release of DHA induced ferroptosis through lipid peroxidation and GSH depletion, enhancing oxidative stress. Combined with irradiation, DHA@MFn achieved superior tumor ablation through synergistic ferroptosis, photothermal effects, and minimal systemic toxicity compared to free DHA, MFn alone, or their combinations with irradiation.Conclusion: This multifunctional biomimetic nanoplatform presents a promising strategy for precise, multimodal ovarian cancer therapy. By integrating controlled drug delivery, catalytic Fenton-like reactions, and synergistic radiotherapy, DHA@MFn demonstrates significant potential for clinical translation in targeted cancer treatment.
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JOURNAL OF BIOCHEMICAL AND MOLECULAR TOXICOLOGY
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2026
·Vol. 40
·期 1
·e70661
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IF 2.8
Li Yao,Xin-ze Qiu,Jun Zou,Jing-rong Liang,Meng-bin Qin,Jin-xiu Zhang,Peng Peng,Jie-an Huang
Metabolic dysfunction-associated steatotic liver disease (MASLD) has become a leading cause of chronic liver disease with no available therapies. Currently, the pathogenesis of MASLD remains to be further elucidated. Ferroptosis and ferroptosis-related genes may play a vital role in the development of MASLD. Thus, this study investigated the role of heme oxygenase-1 (HMOX1/HO-1) in ferroptosis associated with MASLD. Here, we applied bioinformatics to identify ferroptosis-related genes. HMOX1 expression was validated by immunohistochemistry. Mice fed a methionine-choline-deficient diet for 8 weeks were treated with hemin, followed by biochemical and histological analyses. HL7702 cells were transfected to overexpress HMOX1, exposed to oleic acid, and treated with erastin or AZD1480. Iron, ROS, lipid peroxidation, and mitochondrial damage were assessed by ELISA, flow cytometry, and electron microscopy. Western blotting explored molecular mechanisms. HMOX1 was identified as a ferroptosis-related hub gene in MASLD datasets and was decreased in patient liver tissues. MCD-fed mice developed hepatic steatosis with elevated ALT, AST, TG, LDL, Fe²⁺, MDA, and ROS, along with reduced HMOX1 and GSH. Hemin ameliorated MASLD and inhibited ferroptosis. Cell experiments showed JAK/STAT pathway activation in MASLD. HMOX1 upregulation reduced lipid peroxidation, inhibited ferroptosis, and downregulated JAK/STAT, whereas erastin reversed these effects. AZD1480 reversed the effects of erastin and improved MASLD. Collectively, our results suggest that HMOX1 protects against MASLD by suppressing ferroptosis through JAK/STAT pathway inhibition.
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JOURNAL OF NANOBIOTECHNOLOGY
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2026
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IF 15
Lin Lingting,Chen Binyu,Yang Yourui,Deng Ruocheng,Niu Wenfei,Liu Jian,Xu Wei,Li Hua
Background Proteolysis-targeting chimeras (PROTACs) have emerged as a promising cancer therapeutic approach by targeting protein degradation to address undruggable targets and drug resistance associated with conventional therapies, yet their clinical translation is hindered by poor solubility and non-specific toxicity. Additionally, tumor heterogeneity and biological complexity frequently limit the efficacy of monotherapies, necessitating the development of multifunctional delivery systems. Results We engineered a dual microenvironment-responsive albumin to integrate conditional PROTAC activation with metabolic starvation and ferroptosis for synergistic antitumor efficacy within a unified therapeutic cascade. Ferrocene (Fc)-modified human serum albumin (HSA) via coupling chemistry was electrostatically complexed with glucose oxidase (GOD) and co-assembled with an azobenzene (AZO)-caged ARV-771 prodrug to yield HSA-Fc-GOD@ARV-771(AZO) nanoparticles that exhibited pH-triggered disassembly in acidic tumor environments. the released GOD consumes glucose and oxygen to generate hydrogen peroxide while inducing metabolic starvation and exacerbating hypoxia. The intensified hypoxia triggers nitroreductase to cleave the prodrug linker and release the active ARV-771, which subsequently degrades bromodomain containing protein 4. This degradation directly suppresses tumor cell proliferation and downregulates glutathione peroxidase 4 expression to sensitize cancer cells to oxidative damage. Concurrently, the ferrocene component converts the generated hydrogen peroxide into hydroxyl radicals via the Fenton reaction to amplify lipid peroxidation and ferroptotic cell death. The nanoplatform suppressed lung cancer cell viability to 10.8% in vitro and achieved 94.3% tumor growth inhibition in xenograft models without observable systemic toxicity. Conclusions This study demonstrates a precision therapeutic paradigm. It exploits tumor microenvironment characteristics to couple conditional drug activation with starvation and ferroptosis. This strategy offers a translatable framework for next generation’s cancer treatment. Graphical
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JOURNAL OF CONTROLLED RELEASE
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2026
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IF 12.4
Weiqi Zhang,Linjia Chen,Yahui Dong,Yinghua Zeng,Yongyu Chen,Yue Liu,Jingru Wang,Fujun Shi
Triple-negative breast cancer (TNBC) remains a formidable clinical challenge due to the lack of druggable targets and intrinsic resistance to conventional therapies. Ferroptosis, an iron-dependent form of regulated cell death driven by lipid peroxidation, represents a promising therapeutic vulnerability in TNBC. Here, we identify solute carrier family 7 member 5 (SLC7A5) as a ferroptosis-suppressing prognostic target, and develop a tumor microenvironment (TME)-responsive camptothecin (CPT)-peptide conjugates (CPCs) nanoassembly for in situ delivery of the SLC7A5 inhibitor JPH203 to TNBC. The CPCs integrate an active tumor targeting motif, a CPT-based hydrophobic core that drives self-assembly, and a gelatinase-cleavable linker for enzyme-responsive disassembly. Upon TME-triggered release, JPH203 effectively blocks leucine uptake, suppresses mTORC1 signaling, disrupts iron and redox homeostasis, and synergizes with mitochondrial reactive oxygen species to induce potent ferroptosis, achieving an 81.2% tumor growth suppression rate in orthotopic 4 T1 models with favorable biosafety. Importantly, CPCs-JPH promotes dendritic cell maturation, activates CD8 + T-cell responses, and significantly improves survival outcomes in orthotopic 4 T1 tumor-bearing mice. This work establishes a multifunctional and enzyme-responsive nanoplatform that harnesses ferroptosis to overcome therapeutic resistance while concurrently engaging innate and adaptive immunity in TNBC.
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