Advanced Science
·
2024
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IF 14.3
Yu Li,Hongji Li,Keying Zhang,Chao Xu,Jingwei Wang,Zeyu Li,Yike Zhou,Shaojie Liu,Xiaolong Zhao,Zhengxuan Li,Fa Yang,Wei Hu,Yuming Jing,Peng Wu,Jingliang Zhang,Changhong Shi,Rui Zhang,Wenkai Jiang,Nianzeng Xing,Weihong Wen,Donghui Han,Weijun Qin
Conventional androgen deprivation therapy (ADT) targets the androgen receptor (AR) inhibiting prostate cancer (PCa) progression; however, it can eventually lead to recurrence as castration-resistant PCa (CRPC), which has high mortality rates and lacks effective treatment modalities. The study confirms the presence of high glutathione peroxidase 4 (GPX4) expression, a key regulator of ferroptosis (i.e., iron-dependent program cell death) in CRPC cells. Therefore, inducing ferroptosis in CRPC cells might be an effective therapeutic modality for CRPC. However, nonspecific uptake of ferroptosis inducers can result in undesirable cytotoxicity in major organs. Thus, to precisely induce ferroptosis in CRPC cells, a genetic engineering strategy is proposed to embed a prostate-specific membrane antigen (PSMA)-targeting antibody fragment (gy1) in the macrophage membrane, which is then coated onto mesoporous polydopamine (MPDA) nanoparticles to produce a biomimetic nanoplatform. The results indicate that the membrane-coated nanoparticles (MNPs) exhibit high specificity and affinity toward CRPC cells. On further encapsulation with the ferroptosis inducers RSL3 and iron ions, MPDA/Fe/RSL3@M-gy1 demonstrates superior synergistic effects in highly targeted ferroptosis therapy eliciting significant therapeutic efficacy against CRPC tumor growth and bone metastasis without increased cytotoxicity. In conclusion, a new therapeutic strategy is reported for the PSMA-specific, CRPC-targeting platform for ferroptosis induction with increased efficacy and safety.
研究领域:
纳米技术
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癌症生物学
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药学
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生物医学工程
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DOI
PubMed
高影响因子
ACS Nano
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2022
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IF 18.027
Ke Li,Chuanchuan Lin,Menghuan Li,Kun Xu,Ye He,Yulan Mao,Lu Lu,Wenbo Geng,Xuemin Li,Zhong Luo,Kaiyong Cai
Ferroptosis is a recently discovered route of regulated cell death that offers the opportunities for the treatment of chemotherapy-resistant tumor indications, but its efficacy can be affected by the glutathione peroxidase 4 (GPX4) and ferroptosis suppressor protein 1 (FSP1) antioxidant mechanisms, posing significant challenges for its clinical translation. In this study, we report a Cu-tetra(4-carboxyphenyl)porphyrin chloride(Fe(III)) (Cu-TCPP(Fe)) metal organic framework (MOF)-based nanosystem for the efficient incorporation of Au nanoparticles (NPs) and RSL3, which can demonstrate enzyme-like activities to universally suppress the antiferroptotic pathways in tumor cells for amplifying ferroptotic damage. Herein, Cu-TCPP(Fe) MOF nanosheets were integrated with Au NPs via in situ nucleation and loaded with RSL3 via π–π stacking, which were eventually modified with polyethylene glycol (PEG) and iRGD for tumor-targeted drug delivery. Specifically, the Au NPs can demonstrate glucose oxidase-like activities for efficient glucose depletion, thus disrupting the pentose phosphate pathway to impede reduced glutathione (GSH) biosynthesis and prevent the recycling of coenzyme Q10 (CoQ10) to CoQ10H2, while Cu species can oxidize GSH into oxidized glutathione (GSSG). These nanocatalytic activities can lead to the simultaneous inhibition of the GPX4/GSH and FSP1/CoQ10H2 pathways and cooperate with the GPX4-deactivating function of RSL3 to cause pronounced ferroptotic damage, thereby providing a strong rationale for the application of ferroptosis therapy in the clinic.
研究领域:
癌症生物学
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纳米技术
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治疗学
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细胞死亡机制
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DOI
PubMed
高影响因子
JOURNAL OF AGRICULTURAL AND FOOD CHEMISTRY
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2026
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IF 6.7
Ke-xin Cao,Zhi-yuan Xia,Yuan-zhi Cheng,Yan-ping Feng,Meng Liu,Jia-cheng Yang,Yu-xuan Huang,Zhang-chao Deng,Gang Zuo,Xin Gen Lei,Lv-hui Sun
The present study investigated the protective effects and molecular mechanisms of nanoselenium (Nano-Se) against heat stress-induced reproductive damage in Hainan Wenchang roosters. Compared with sodium selenite, Nano-Se more effectively improved sperm quality, enhanced activities of testicular antioxidant enzymes (glutathione peroxidase and thioredoxin reductase), and attenuated lipid peroxidation, as indicated by decreased malondialdehyde and protein carbonyl levels under heat stress conditions. Nano-Se also inhibited testicular cell apoptosis and preserved blood-testis barrier integrity. Notably, Nano-Se reduced testicular iron accumulation and suppressed ferroptosis, as evidenced by increased expression of SLC7A11, GPX4, and NQO1 and decreased expression of DMT1 and ACSL4. Consistently, in heat-stressed GC-2 spd(ts) cells, Nano-Se attenuated ferroptosis by reducing iron accumulation, lipid peroxidation, and mitochondrial damage. Mechanistically, the protective effects of Nano-Se were associated with modulation of the SLC7A11/GSH/GPX4 axis and enhanced GPX4 expression. These findings indicate that Nano-Se is an effective antiferroptotic selenium source for mitigating heat stress-induced male reproductive damage.
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PubMed
高影响因子
Journal of Inflammation Research
·
2025
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IF 4.1
Huiqin Zhou,Yunjia Peng,Xinhua Huo,Bingqing Li,Huasheng Liu,Jian Wang,Gaihua Zhang
Background: Ferroptosis is a form of programmed cell death triggered by iron-dependent lipid peroxidation, characterized by iron accumulation and elevated reactive oxygen species (ROS), leading to cell membrane damage. It is associated with a variety of diseases. However, the cellular and molecular links between ferroptosis, immune inflammation, and the brain-peripheral blood axis in Alzheimer’s disease (AD) remain unclear.Methods: We integrated bulk RNA-seq data from AD brain tissue and peripheral blood and refined the screening of AD candidate genes through differential gene expression analysis, weighted gene co-expression network analysis (WGCNA), and other approaches. Additionally, we analyzed single-cell RNA-seq (scRNA-seq) data from AD patients’ brain tissue and peripheral blood, combined with scRNA-seq data from experimental autoimmune encephalomyelitis (EAE) mouse brain tissue. This enabled us to explore AD-related molecular mechanisms from a cell-type-specific perspective. Finally, candidate genes were validated in ferroptosis models using reverse transcription quantitative PCR (RT-qPCR) and immunofluorescence methods.Results: Bulk RNA-seq analysis identified SLC11A1, an inflammatory gene associated with AD. Single-cell RNA-seq analysis further revealed that SLC11A1 expression was significantly elevated in the pro-inflammatory (M1-type) microglia and peripheral blood monocytes in AD. Moreover, we identified a microglial subpopulation in AD M1-type microglia that was highly associated with ferroptosis. This subpopulation simultaneously expressed characteristic markers of peripheral blood monocytes, suggesting that these cells may originate from peripheral blood monocytes, thereby triggering neuroinflammation through the ferroptosis pathway. Cell experiments confirmed that SLC11A1 was significantly upregulated in inflammatory microglia induced by ferroptosis.Conclusion: This study reveals the key role of SLC11A1 in AD, particularly in the context of ferroptosis and immune inflammation. It provides a novel molecular mechanistic perspective and offers potential targets for future therapeutic strategies.
研究领域:
神经科学
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分子生物学
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生物信息学
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PubMed
高影响因子
INFLAMMATION RESEARCH
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2025
·Vol. 74
·期 1
·1-19
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IF 5.4
Weng Xiuhong,Wang Simin,Wang Qing,Wei Mingbo,Cheng Bo
Background Primary Sjögren’s syndrome (pSS) is an autoimmune disease characterized by xerostomia and autoimmune sialadenitis. Interferon-γ (IFN-γ) induces ferroptosis in salivary gland epithelial cells (SGECs), leading to salivary gland (SG) hypofunction. We previously demonstrated the beneficial effects of melatonin (MLT) in alleviating SG dysfunction and inflammation in a pSS animal model. However, the precise underlying mechanism remains unclear. Methods Female NOD/ltj and ICR mice were used as the pSS mouse model and control group, respectively. MLT was administered via intraperitoneal injection to NOD/ltj mice to detect its effect on ferroptosis in SGs. Primary human SGECs and A253 cells were treated with IFN-γand ferroptosis inducers, with or without MLT. Results Exogenous MLT alleviated pathological SG alterations and promoted saliva production through inhibiting SGEC ferroptosis. MLT inhibited SGEC ferroptosis induced by IFN-γ and ferroptosis inducers via nuclear factor erythroid 2-related factor 2/heme oxygenase-1/glutathione peroxidase 4 (NRF2/HO-1/GPX4) pathway activation. Moreover, MLT suppressed the nuclear factor-kappa B (NF-κB) pathway, which is triggered by ferroptosis in SGECs. Nevertheless, ML385-mediated NRF2 inhibition abrogated the antiferroptotic protective effects of MLT on SGECs. Conclusions MLT inhibits SGEC ferroptosis through NRF2/HO-1/GPX4 pathway activation and thus attenuates ferroptosis-triggered NF-κB activity. Melatonin represents a potential therapeutic approach for pSS owing to its capacity to regulate ferroptosis.
研究领域:
免疫学
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细胞生物学
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医学
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DOI
PubMed
高影响因子
JOURNAL OF AGRICULTURAL AND FOOD CHEMISTRY
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2025
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IF 6.2
Cong Zhang,Yangkun Xiong,Mingyang Gong,Haixia Zhao,Shan Li,Xin Chen,Xiaochuan Ye,Zhenpeng Qiu
Hyperuricemic nephropathy, a common subtype of chronic kidney disease (CKD), has become an important global public health issue and is closely related to the dramatic increase in fructose consumption. Pachymic acid, the primary active ingredient of the edible fungal herb Poria cocos, has demonstrated the protective capacity against renal injury, but its beneficial effect on hyperuricemic nephropathy remains unclear. In this study, a fructose-diet-induced hyperuricemia nephropathy mouse model was established to reveal the efficacy of pachymic acid in inhibiting hyperuricemic nephropathy the progression. Our results showed that pachymic acid restored abnormal renal function indexes and pathological manifestations such as tubular dilatation and glomerular fibrosis in fructose-fed mice. Transcriptome sequencing results showed marked alterations in glutathione metabolism and ferroptosis signaling pathways in the kidneys of fructose-fed mice after pachymic acid treatment. Mechanistically, pachymic acid activated the Nrf2/GPX-4 signaling pathway by directly binding to Nrf2 and promoting its nuclear translocation, thereby inhibiting ferroptosis, oxidative stress, and inflammatory responses in the kidneys of fructose-fed mice. Consistent results were observed in uric acid-treated HK-2 cells. Notably, both Nrf2 inhibitor ML385 and GPX-4 inhibitor RSL3 treatments reversed the protective effects of pachymic acid against renal injury by suppressing ferroptosis in vitro and in vivo. Summary, our study provides compelling evidence that pachymic acid ameliorates renal injury in fructose-fed mice by inhibiting ferroptosis through targeted activating an Nrf2/GPX-4 pathway, suggesting that dietary supplementation with Poria cocos or pachymic acid might be an effective strategy for CKD prevention, particularly in the subtype of fructose-diet-driven hyperuricemic nephropathy.
研究领域:
药理学
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肾脏病学
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生物化学
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分子生物学
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营养学
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药物化学
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DOI
PubMed
高影响因子
Redox Biology
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2025
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IF 11.9
Xue Shi,Yun Zhao,Hong-Yu Gao,Wei Yang,Jun Liao,Hui-Han Wang,Xiao-Tian Wang,Wei Yan
Diffuse large B cell lymphoma (DLBCL) is a common hematologic malignancy. NFS1 cysteine desulfurase, as a rate-limiting enzyme in the iron-sulfur cluster (ISC) biogenesis, has been reported to be associated with tumor progression. However, the role of NFS1 in DLBCL remains elusive. Here, we showed an upregulation of NFS1 in DLBCL tumor tissues. Knockdown of NFS1 decreased the cell viability and enhanced LDH levels in DLBCL cells. Animal experiments further indicated that downregulation of NFS1 suppresses tumor growth in vivo. NFS1 knockdown increased the lipid reactive oxygen species (ROS) level in cells, and this promotional effect was reversed by ferroptosis inhibitors, but not influenced by other types of cell death inhibitors. This result suggested that NFS1 depletion-impaired cell viability is associated with ferroptosis. Silenced NFS1 aggravated ferroptosis inducers caused cell viability inhibition, lactate dehydrogenase (LDH), and lipid ROS levels enhancement, while the addition of ferroptosis inhibitors abated these trends. Moreover, catalytic residue mutation of NFS1 did not affect its protein expression but decreased the cell viability, which was promoted by NFS1 upregulation, indicating that the protective effect of NFS1 in DLBCL cells was related to its catalytic activity. Further results showed that frataxin (FXN), the upstream activator of NFS1, reduced the cell viability in NFS1 upregulated cells. Consistent with NFS1, FXN silencing aggravated erastin-induced cell viability inhibition and LDH level enhancement. Silencing NFS1 or FXN inhibited the level of iron ions storage-related proteins but promoted the level of transport-related proteins. In addition, silenced NFS1 or FXN displayed an inhibition effect on protein expression of DNA polymerases, but a promotion trend in the phosphorylation of DNA damage markers. In conclusion, we demonstrated that ISC-related proteins NFS1 and FXN protect DLBCL cells from ferroptosis and DNA damage, thus exhibiting an essential role in DLBCL progression.
研究领域:
肿瘤学
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分子生物学
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血液病学
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细胞生物学
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氧化应激
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PubMed
高影响因子
Journal of Inflammation Research
·
2025
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IF 4.1
Yi-Xuan Zeng,Ni-Ren Li,Bing-Ying Deng,Yu-Feng Gu,Si-Fan Lu,Yi Liu
Background Ulcerative colitis is a chronic intestinal disease linked to intestinal barrier damage, ferroptosis and dysbiosis. Coix lacryma-jobi is a natural food with food-medicine homology, whose seed-derived oil (Coix seed oil, CSO) has been shown anti-inflammatory activity in vitro. Here, the effects and mechanisms of CSO on ulcerative colitis (UC) in vivo are systematically investigated.Methods Firstly, the UC mice was replicated by 3% DSS, and assessed the efficacy of CSO by observing the fecal occult blood, colon length, DAI score and pathological histomorphological changes of colon tissues. The anti-inflammatory and barrier-protective effects of CSO were observed by AB staining and qRT-PCR. Secondly, the biological targets of CSO were obtained from TCMSP database and Swiss Target Prediction database, ferroptosis targets were downloaded from FerrDb platform, and UC-related disease targets were obtained from GEO database, and the intersection of the above three was taken to obtain “CSO-UC-Ferroptosis” intersection targets, which were analysed by GO and KEGG enrichment, GSEA analysis, and immune cell infiltration and validation. Finally, the core genes of “CSO-UC-Ferroptosis” were molecular docking with the potential active components of CSO. In order to further verify the effect of CSO on ferroptosis, the GPX4 agonist RSL-3 was used to stimulate mice in vivo, and the levels of Iron, MDA and SOD were measured, and immunohistochemistry was used to detect the effects of tight junction proteins and the “CSO-UC-Ferroptosis” core protein in mice. Besides, the effect of CSO was further evaluated by observing the intercellular junctions of the colon tissues of each group under electron microscope. In addition, 16sRNA sequencing was performed on the intestinal contents of the mice to observe the effects of CSO on the intestinal flora of UC mice.Results CSO improved physiological parameters, reduced inflammation response and intestinal barrier damage, regulated ferroptosis, and restored gut microbiota balance in UC mice. Bioinformatics results showed that G6PD, ABCC1 were core targets at the intersection of CSO, UC and ferroptosis, which also demonstrated the similar expression of the core genes in DSS-induced UC mice models in vivo.Conclusion Our findings demonstrate for the first time that CSO ameliorated UC by regulating intestinal barrier damage, ferroptosis and the gut microbiota in DSS-induced mice, suggesting that CSO as a promising candidate for UC treatment and warranting further investigation.
研究领域:
药理学
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免疫学
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分子生物学
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微生物学
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DOI
PubMed
高影响因子
Marine Drugs
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2025
·Vol. 23
·期 1
·49
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IF 5.4
Zi-Han Xu,Ming-Min Xie,Chun-Lan Xie,Xian-Wen Yang,Jun-Song Wang
Neuroinflammation and neuronal cell death are leading causes of death in the elderly and underlie various neurodegenerative diseases. These diseases involve complex pathophysiological mechanisms, including inflammatory responses, oxidative stress, and ferroptosis. Compounds derived from deep-sea fungi exhibit low toxicity and potent neuroprotective effects, offering a promising source for drug development. In this study, we isolated 44 natural products from deep-sea-derived fungi and identified isobisvertinol (17) as a compound with anti-inflammatory and ferroptosis-inhibiting effects. Using LPS-induced microglial inflammation and RSL3-induced neuronal ferroptosis models, we found that17targets TLR4 to provide neuroprotection. Molecular docking studies revealed that17inhibits TLR4 activation by occupying the hydrophobic pocket at the TLR4-MD2 binding site. Additionally,17suppresses TLR4, reducing p38 MAPK phosphorylation, and inhibits ferroptosis by decreasing lipid peroxidation and modulating mitochondrial membrane potential. Metabolomic analysis showed that17rescues alterations in multiple metabolic pathways induced by RSL3 and increases levels of antioxidant metabolites, including glutamine, glutamate, and glutathione. In summary, our results indicate that isobisvertinol (17) targets TLR4 in neural cells to reduce inflammation and inhibit p38 MAPK phosphorylation, while regulating metabolic pathways, mainly GSH synthesis, to provide antioxidant effects and prevent ferroptosis in neurons.
研究领域:
神经科学
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药理学
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免疫学
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分子生物学
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DOI
PubMed
高影响因子
FREE RADICAL BIOLOGY AND MEDICINE
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2024
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IF 7.1
Deshan Yao,Liuxiang Bao,Sichuan Wang,Meng Tan,Yuanyuan Xu,Tianxu Wu,Zhengang Zhang,Kaizheng Gong
Ischemia-reperfusion (I/R) injury, a multifaceted pathological process, occurs when the prolongation of reperfusion duration triggers ferroptosis-mediated myocardial damage. Isoliquiritigenin (ISL), a single flavonoid from licorice, exhibits a wide range of pharmacological impacts, but its function in ferroptosis caused by myocardial I/R injury remains unclear. This study delved into the protective effect of ISL on myocardial I/R injury-induced ferroptosis and its mechanism. Neonatal mouse cardiomyocytes (NMCM) underwent hypoxia/reoxygenation (H/R) to simulate the pathological process of myocardial I/R. ISL significantly attenuated H/R-triggered production of reactive oxygen species in NMCM, reduced the expression of malondialdehyde and the activity of lactate dehydrogenase, enhanced superoxide dismutase and catalase activity, and increased the expression of nuclear factor E2-related factor 2 (Nrf2) and its downstream heme oxygenase 1 (HO-1), thereby mitigating oxidative stress damage. CCK8 experiment revealed that the ferroptosis inhibitor Ferrostatin-1 significantly improved myocardial cell viability after 24 h of reoxygenation, and ISL treatment showed a similar effect. ISL reduced intracellular free iron accumulation, up-regulated glutathione peroxidase 4 (GPX4) and solute carrier family 7 member 11 (SLC7A11) expression, and inhibited lipid peroxidation accumulation, thereby alleviating ferroptosis. The Nrf2-specific inhibitor ML385 counteracted ISL's defensive role against H/R-triggered oxidative stress damage and ferroptosis. In vivo experiments further confirmed that by regulating the translocation of Nrf2 into the nucleus, ISL treatment increased the levels of HO-1, GPX4, and SLC7A11, inhibited the expression of ACSL4, Drp1 to exert the antioxidant role, alleviated mitochondrial damage, and ferroptosis, ultimately reducing myocardial infarction area and injury induced by I/R. ML385 nearly abolished ISL's protective impact on the I/R model by inhibiting Nrf2 function. In summary, ISL is capable of mitigating oxidative stress, mitochondrial damage, and cardiomyocyte ferroptosis caused by I/R, thereby reducing myocardial injury. A key mechanism includes triggering the Nrf2/HO-1/SLC7A11/GPX4 pathway to prevent oxidative stress damage and cardiomyocyte ferroptosis caused by I/R.
研究领域:
药理学
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心脏病学
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分子生物学
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细胞生物学
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PubMed
高影响因子
BIOCHEMICAL PHARMACOLOGY
·
2025
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IF 5.6
Jiajian Wang,Lanqing Zhang,Runfang Li,Rui Yang,Fan Yang,Fei Yu,Jihong Zhang
TP53, the most frequently mutated gene in human cancers, undergoes a functional transformation from a tumor suppressor to an oncoprotein, thereby enhancing tumor aggressiveness, metastatic potential, and resistance to therapy. Given the prevalence of p53 mutations in cancer, the reactivation of wild-type p53 function presents a compelling therapeutic strategy for these malignancies. In this study, we identified gambogic acid (GA), a natural compound, as a potent reactivator of mutant p53 transcriptional activity. Immunofluorescence and co-immunoprecipitation assays revealed that GA treatment upregulates wild-type p53 expression while depleting mutant p53 in cancer cells. The time-dependent restoration of p53′s DNA-binding capacity and transcriptional regulatory activity by GA was further demonstrated through EMSA and ChIP. Consequently, GA robustly induced the expression levels of canonical p53 downstream target genes, confirming functional restoration of p53 signaling. In addition, GA synergizes with RSL3, a GPX4 inhibitor, to promote ferroptosis in mutant p53 cancer cells in both cellular and animal studies. In summary, our findings identify GA as a promising compound that reactivates mutant p53 through thiol modification, restoring its wild-type function and inducing ferroptosis in p53-mutant cancer cells. The findings of this study establish a foundational rationale and new perspectives for a mutant p53-directed therapeutic paradigm in oncology.
研究领域:
肿瘤学
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分子生物学
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药理学
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癌症生物学
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药物发现
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DOI
PubMed
高影响因子
Journal of Advanced Research
·
2026
·
IF 17.1
Weichen Dong,Wenxin Zhang,Li Huang,Lulu Xiao,Yuanfei Luo,Linying Yuan,Yike Jiang,Anyu Liao,Hongting Zhao,Zhihui Liu,Jia Wang,Ying Zhao,Yulong Cai,Mengna Peng,Dong Yang,Yi Xie,Kuanyu Li,Wusheng Zhu
Introduction Cardiolipins (CLs) are mitochondria-specific phospholipids critically involved in neurological disorders. However, their role in cerebral ischemia/reperfusion (I/R) injury remains largely underexplored. Objectives This study aimed to characterize CL alterations following cerebral I/R injury, identify potential mechanisms underlying CL loss, and investigate the pathophysiological effects of these changes. Methods Ischemic stroke was modeled by using middle cerebral occlusion/reperfusion (MCAO/R) in mice and oxygen-glucose deprivation/reoxygenation (OGD/R) in vitro . CL alterations following cerebral I/R injury were evaluated through lipidomic analysis and fluorescent staining. The role of extracellular vesicles (EVs) in CL release was investigated. The effects of CL-targeting peptide SS-31 on CL release and homeostasis were assessed, and underlying mechanisms were explored by analyzing neuronal autophagy and ferroptosis. Plasma CL levels in stroke patients were also measured to elucidate clinical relevance. Results Significant CL depletion and acyl chain remodeling were observed in peri -infarct brain tissues. EV-mediated release was identified as one of the mechanisms of CL loss, and inhibiting EV release restored neuronal CL levels. SS-31 inhibits CL release, preserves CL content, and subsequently restores CL homeostasis. Restoring CL homeostasis attenuated cerebral I/R injury by suppressing neuronal ferroptosis. Mechanistically, SS-31 downregulated autophagy-associated genes, with ATG5 identified as the crucial target. Activating autophagy or overexpressing ATG5 reversed the protective effects of SS-31. Clinically, plasma CL levels in patients undergoing endovascular treatment correlated with 90-day functional outcomes. Conclusion Our findings establish CL preservation as a novel neuroprotective strategy, in which SS-31 mitigates I/R injury by restoring CL homeostasis and ameliorating ATG5-mediated autophagy-dependent neuronal ferroptosis, offering a novel therapeutic avenue for stroke.
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高影响因子
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