Natural Products and Bioprospecting
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2026
·Vol. 16
·期 1
·34
·
IF 5.8
Liu Qiuyu,Cong Mengjing,Gao Chenghai,Liu Yonghong,Wang Junfeng,Wang Xueni
Prostate cancer (PCa) remains one of the most common malignant tumors among men worldwide, typically relying on the androgen receptor (AR) signaling pathway. Inducing ferroptosis, a novel form of iron-dependent cell death, represents a promising strategy; however, its regulation by AR signaling is complex. The molecular chaperone heat shock protein 70 (HSP70) is critical for AR stability and function, yet its role as a therapeutic target in this context is underexplored. The anti-proliferative effect of the compound nidurufin (Nid) was assessed across PCa cell lines using MTT, clonogenic, and 3D spheroid assays. Ferroptosis was evaluated by transmission electron microscopy, reactive oxygen species (ROS) detection, and lipid peroxidation analysis. Mechanistic insights were gained through Western blot, qPCR, immunofluorescence, ChIP-qPCR, molecular docking, and cellular thermal shift assay (CETSA). In vivo efficacy was validated in a zebrafish xenograft model. Nid exhibited potent, selective anti-proliferative activity against AR-positive PCa cells, particularly 22Rv1 (IC₅₀ = 10.30 μM), and induced ferroptosis characterized by mitochondrial shrinkage and ROS accumulation. Mechanistically, Nid did not bind to AR, but it directly bound to HSP70, disrupting its chaperone function and leading to AR protein destabilization and transcriptional downregulation. This consequently suppressed the expression of the AR-target gene membrane-associated O-acyltransferase domain protein 2 (MBOAT2), a key ferroptosis suppressor enzyme. ChIP-qPCR confirmed AR directly binds the MBOAT2 promoter, and Nid treatment reduced this enrichment. In vivo, Nid significantly inhibited tumor growth and metastasis in a zebrafish xenograft model. Our study identifies Nid as a novel HSP70-targeted compound that triggers ferroptosis by disrupting the HSP70-AR-MBOAT2 axis. This work not only reveals a previously unrecognized connection between protein chaperone function and ferroptotic susceptibility but also positions HSP70 as a compelling therapeutic target for overcoming AR-pathway dependency in PCa. Graphical
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BME Frontiers
·
2026
·
IF 9.1
Zengfeng Guo,Ningfeng Zhang,Junshen Huang,Wang Zhang,Yawei Hu,Shaochu Chen,Ming Gong,Jianhua Zhou,Jiancheng Yang,Jiawen Wu
Objective: This study aimed to investigate the protective effects and underlying mechanisms of baicalein against iron overload-induced osteoblast dysfunction and bone loss. Impact Statement: This research is the first to demonstrate that baicalein, a natural flavonoid, functions as a dual-action agent combining iron chelation and antioxidation to prevent iron overload-induced ferroptosis in osteoblasts, offering a novel therapeutic strategy for iron overload-related osteoporosis. Introduction: Iron overload contributes to osteoblast damage and osteoporosis through ferroptosis, an iron-dependent cell death pathway. Current treatments fail to simultaneously address iron accumulation and bone loss, highlighting the need for effective dual-function therapies. Methods: Using iron dextran-treated MC3T3-E1 osteoblasts and a murine iron overload model, we assessed the effects of baicalein on cell viability, osteogenic differentiation, ferroptosis markers, and the nuclear factor erythroid 2-related factor 2 (Nrf2)/glutathione peroxidase 4 (GPX4) pathway via biochemical assays, Western blot, and micro-computed tomography. Genetic and pharmacological inhibition of Nrf2 were applied to validate the mechanism. Results: Baicalein chelated iron, scavenged reactive oxygen species, and suppressed ferroptosis in osteoblasts, restoring differentiation under iron overload. It activated Nrf2 nuclear translocation and upregulated GPX4/solute carrier family 7-member 11 (SLC7A11) expression. In mice, baicalein reduced iron deposition, oxidative stress, and bone loss, and these effects were abolished by Nrf2 inhibition. Conclusion: Baicalein alleviates iron overload-induced osteoblast ferroptosis and osteoporosis by activating the Nrf2/GPX4 pathway, supporting its clinical potential as a therapeutic agent for iron-related bone disorders.
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FREE RADICAL BIOLOGY AND MEDICINE
·
2026
·
IF 8.2
Yi Chen,Zhaoyu Liu,Zesen Mai,Yongbing Zhou,Huiwen Wen,Gaowen Qu,Runhao Zeng,Jianfu Zhao,Dongmei Zhu,Yuxiong Lai,Xue Liang
Non-small cell lung cancer (NSCLC) remains a lethal malignancy due to therapy resistance and recurrence. Ferroptosis, a regulated form of cell death, is a promising strategy to overcome cancer drug resistance, yet its mechanisms remain incompletely defined. Here, we report that Immediate Early Response 3 (IER3) is significantly upregulated in NSCLC tumors and linked to advanced stage and poor prognosis. Using IER3-overexpressing and knockout models in A549 and H1299 cells, we found that IER3 promotes NSCLC cell proliferation, migration, and invasion by suppressing ferroptosis. Conversely, IER3 knockout induced ferroptosis and reduced malignancy—effects reversed by the ferroptosis inhibitor Fer-1. Mechanistically, IER3 sustained AKT phosphorylation to inactivate GSK3β, both blocking GSK3β-dependent proteasomal degradation of NRF2 and enhancing its nuclear translocation, which collectively led to the transactivation of downstream ferroptosis-suppressive gene programs. This program maintained glutathione homeostasis, sequestered labile iron, scavenged ROS, and ultimately inhibited lipid peroxidation to counter ferroptosis. Rescue assays confirmed NRF2 overexpression or AKT/GSK3β activation reversed IER3 knockout-induced ferroptosis and viability loss. Additionally, low-IER3 NSCLC tumors were more sensitive to clinical/preclinical agents targeting survival/stress pathways. Collectively, our findings establish IER3 as an NSCLC oncogenic driver—suppressing ferroptosis via AKT/GSK3β/NRF2 to sustain malignancy—highlighting its potential as a prognostic biomarker and therapeutic target for improved NSCLC outcomes.
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JOURNAL OF NANOBIOTECHNOLOGY
·
2026
·
IF 12.6
Song Wanli,Zhao Chuanyi,Mai Youqing,Zhang Guangrong,Kang Wenyue,Zheng Xuanjun,Yuan Qingpeng,Chen Zeyang,Zhong Chengxun,Tang Junbao,Fu Duoyi,Zhai Tiantian,Ling Kai,Jiang Hongyan
Low-dose X-ray-activated radiodynamic therapy (RDT) is a promising strategy for precision oncology. However, its therapeutic efficacy is limited by tumor radioresistance and insufficient generation of reactive oxygen species (ROS). Here, we describe a biomimetic lutetium-coordinated black phosphorus nanosheet platform (BPNS@Lu 3+ /Lap-CMV) capable of initiating a tripartite synthetic lethality cascade upon low-dose irradiation. Through a single coordination strategy utilizing high atomic number (high-Z) Lu 3+ ions, the nanoplatform simultaneously stabilizes the black phosphorus scaffold, functions as an efficient X-ray antenna, and integrates a pH-responsive gate for the controlled release of β-lapachone (Lap). Additionally, surface camouflage using cancer cell membrane vesicles (CMV) enables homologous tumor targeting and reduces clearance by the reticuloendothelial system. A multi-pathway therapeutic cascade is initiated upon exposure to low-dose X-ray. First, Lu 3+ -amplified RDT generates a burst of ROS. Second, tumor-overexpressed NAD(P)H: quinone oxidoreductase 1 (NQO1) bioactivates Lap, intensifying redox stress (GSH depletion and H 2 O 2 overproduction) and promoting ferroptosis. Third, co-administration of the PARP inhibitor olaparib (Ola) functionally impairs PARP-mediated DNA repair, thereby converting RDT-induced DNA lesions into lethal damage and promoting apoptosis. Guided by its intrinsic computed tomography-mediated visibility, which revealed peak tumor accumulation at 12 h post-administration, the triple‑combination regimen achieved 85.5% tumor suppression in an orthotopic triple-negative breast cancer model without evident toxicity. This study presents a strategic framework for an intelligent nanoplatform capable of converting low-dose physical energy into biological cascades, thereby systematically disrupting parallel tumor defense mechanisms and broadening the therapeutic scope of radiotherapy. Graphical abstract
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Theranostics
·
2026
·Vol. 16
·期 3
·1262
·
IF 13.3
Yanlan Xie,Huan Wang,Yalan Wang,Jiajie Liu,Jinming Tong,Tao Wu,Li Yin,Chuan Zhang,Long Zhao,Yuan Yong
Background: The pathological hyperglycemic microenvironment in diabetic wounds increases susceptibility to bacterial infections and impairs wound healing. However, despite certain advancements in conventional clinical treatments, the pathological issues have not yet been fundamentally resolved. The mechanism that amplifies ferroptosis through disruption of the bacterial electron transport chain (ETC) results in effective bacterial eradication and facilitates wound healing, thereby offering novel therapeutic potential for the management of diabetic wound infections. Methods: This work designs a multi-enzyme-mimicking Fe-WS 2 @GOx nanozymes by loading glucose oxidase (GOx) onto defect-engineered Fe-WS 2 , which disrupts the bacterial ETC and induces ferroptosis, thereby accelerating diabetic wound healing. Results: During the bacterial infection stage, the Fe-WS 2 @GOx nanozymes with abundant sulfur vacancies can simultaneously mitigate hyperglycemic and alleviate the hypoxic microenvironment. This is achieved through continuously producing substantial amounts of reactive oxygen species (ROS), resulting in endogenous glucose consumption, promoting cyclic accumulation of H 2 O 2 , and ensuring a sustained oxygen supply. Meanwhile, the generated ROS interferes with the bacterial ETC, impedes bacterial energy metabolism and inhibits biosynthesis, ultimately leading to bacterial death. More importantly, at the new tissue proliferation stage, Fe-WS 2 @GOx can promote wound angiogenesis and tissue regeneration by macrophage immunomodulatory effect. Conclusions: Therefore, this study provides a new paradigm strategy for diabetic wound infections therapy by “electron transport chain interference” amplified bacterial ferroptosis.
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MEDIATORS OF INFLAMMATION
·
2026
·
IF 4.2
Zenghui Hao,Jinbao Han,Ting Yao,Zheng Zhao,Wei Fan,Zaiqun Jiang,Yunting Wang,Xiaoqian Yang,Zhilin Xu
Neonatal necrotizing enterocolitis (NEC) is an intestinal disease that occurs in the neonatal period. The purpose of this study was to investigate the role of 5′‐aminolevulinate synthase 2 (ALAS2) in NEC‐induced intestinal injury. In a neonatal mouse, NEC model was induced by high‐osmolarity formula and hypoxia‐cold stress, and ALAS2 expression was significantly downregulated in ileal tissues ( p < 0.01), coinciding with elevated oxidative stress (increased Fe 2+ /malondialdehyde [MDA] and decreased superoxide dismutase [SOD]), inflammation (increased TNF‐α/interferon‐gamma [IFN‐γ]), and ferroptosis activation (increased acyl‐CoA synthetase long‐chain family member 4 [ACSL4] and decreased ferritin heavy chain 1 [FTH1] with mitochondrial shrinkage). In vitro, tumor necrosis factor‐alpha (TNF‐α)/IFN‐γ‐treated intestinal epithelial cell (IEC) exhibited progressive ALAS2 suppression and increased necrosis. Crucially, lentivirus‐mediated ALAS2 overexpression reversed these effects, reducing cell necrosis by 22% while suppressing ferroptosis markers (Fe 2+ accumulation, lipid reactive oxygen species [ROS], and mitochondrial depolarization) and oxidative damage (decreased MDA and restored glutathione [GSH]/catalase [CAT]/SOD). Untargeted metabolomics further revealed ALAS2‐mediated modulation of nutrient metabolism and redox pathways. Collectively, ALAS2 ameliorates NEC by blocking oxidative stress‐driven ferroptosis in IECs, proposing a novel therapeutic target.
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MOLECULAR PHARMACEUTICS
·
2026
·Vol. 23
·期 8
·4341-4359
·
IF 4.9
Zhang Jieke,Li Yafang,Tian Chaoying,Zhang Xiaodi,Guo Jialing,Liu Chenxin,Wu Ligang,Du Bin,Cheng Genyang
Acute kidney injury (AKI) is a clinical syndrome with
high incidence
and mortality involving oxidative stress, ferroptosis, and inflammation,
yet there are no clinically effective interventions. Herein, HA@PDA@EGCG
nanoparticles were constructed using polydopamine (PDA) as carriers,
loaded with epigallocatechin gallate (EGCG) via π-π stacking,
and further surface-modified with hyaluronic acid (HA) through electrostatic
interaction. The nanoparticles had uniform morphology with a size
of approximately 50 nm and an EGCG loading capacity of 15.4 ±
0.8%. They exhibited prominent broad-spectrum antioxidant activity
and hydrogen peroxide-responsive EGCG release, with a cumulative release
rate of 58.2 ± 2.2% within 2 h and close to 80% at 12 h. Cellular
uptake and in vivo distribution confirmed the efficient CD44 receptor-mediated
internalization of the nanoparticles by human kidney-2 (HK-2) cells
as well as renal-targeted accumulation. Reactive oxygen species (ROS)
staining, mitochondrial morphology and apoptosis assays showed that
the nanoparticles effectively scavenged ROS, alleviated mitochondrial
damage, and inhibited cell apoptosis. In a cisplatin-induced in vivo
AKI model, HA@PDA@EGCG significantly restored renal function: blood
urea nitrogen and creatinine decreased to 12.3% and 27.2% of model
group levels, respectively, while alleviating renal pathological damage
and inflammation. Mechanistically, HA@PDA@EGCG inhibited ferroptosis
by downregulating acyl-CoA synthetase long-chain family member 4 (ACSL4)
to suppress lipid synthesis, chelating ferrous ions, and stabilizing
glutathione peroxidase 4 (GPX4) protein. Collectively, HA@PDA@EGCG
achieved renal protection by ameliorating oxidative stress, suppressing
inflammation and inhibiting ferroptosis through multiple pathways,
offering a novel strategy for targeted AKI therapy.
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International Journal of Pharmaceutics-X
·
2026
·
IF 7.9
Yinghong Huang,Yuanyuan Zhao,Yuhong Su,Chudong He,Mengdie Mo,Weijie Zhou,Yang Lu,Fei Yu
Ferroptosis, an iron-dependent programmed cell death process driven by reactive oxygen species (ROS) accumulation, represents a promising therapeutic strategy for breast cancer. However, the efficacy of ferroptosis therapy in breast cancer is often compromised by insufficient intracellular levels of hydrogen peroxide (H 2 O 2 ) and iron ions. To address these problems, we developed pH-responsive nanoparticles comprising a metal–phenolic network (MPN) shell and a bovine serum albumin (BSA) core for the delivery of artesunate (ART) (designated as BAM NPs). The designed BAM NPs aim to amplify oxidative stress and enhance ferroptosis-based therapy for breast cancer. Upon endocytosis by tumor cells, BAM NPs underwent degradation under acidic conditions to release ART and Fe 3+ . Subsequently, the reduction of Fe 3+ to Fe 2+ by glutathione (GSH) initiated the Fenton reaction, which led to aberrant accumulation of ROS. Meanwhile, the endoperoxide bridge of ART could be cleaved by Fe 2+ to further generate carbon-centered radicals (·C). Furthermore, BAM NPs effectively deplete GSH via Fe 3+ /Fe 2+ conversion to inactivate glutathione peroxidase 4 (GPX4), thereby disrupting redox homeostasis and increasing intracellular LPO levels. Both in vitro and in vivo experiments showed that BAM NPs significantly inhibited tumor cell proliferation by inducing robust ferroptosis in tumor cells, leading to a tumor inhibition rate of 83.11%. In summary, the constructed BAM NPs served as a promising tailored nanoplatform for augmenting ferroptosis therapy in breast cancer.
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JOURNAL OF ETHNOPHARMACOLOGY
·
2026
·
IF 6.8
Xin Guo,Bao-Nian Huang,Yu-Han Liu,Yan-Qiu Wang,Huan-Yu Che,Xue-Kun Liu
Ethnopharmacological relevance Crataegus pinnatifida Bunge, a plant used traditionally in herbal medicine for digestive health, is known for its gut-protective properties. Orientin, a natural flavonoid compound abundant in this species, exhibits anti-inflammatory and gut-protective activities. Aim of the study This study examined the therapeutic potential of orientin against ulcerative colitis (UC) and aimed to elucidate its underlying molecular mechanisms. Methods This study established a DSS-triggered UC mouse model. RNA sequencing was carried out to identify key signaling pathways implicated in orientin's therapeutic effects. Disease activity, intestinal barrier integrity, inflammatory responses, ferroptosis, were systematically evaluated. To validate the role of GLUT1 in the pathogenesis of UC, GLUT1-knockdown mice were utilized. Additionally, LPS-stimulated primary intestinal epithelial cells (IECs) were employed to further confirm the protective effects of orientin in vitro. Results RNA sequencing revealed that orientin significantly modulated genes associated with inflammation, ferroptosis, and metabolic pathways. Orientin alleviated DSS-triggered colitis by boosting body weight, preserving colon length, reducing histological damage. GLUT1 deficiency exacerbated intestinal injury, whereas orientin treatment attenuated these effects by regulating the ROS/HIF-1α/GLUT1 signaling axis. Orientin also repressed pro-inflammatory cytokines, neutrophil infiltration, and oxidative stress, while inhibiting the ferroptosis pathway. Moreover, it normalized glycolytic reprogramming by targeting the ROS/HIF-1α/GLUT1 pathway. In vitro studies further confirmed orientin's protective effects on IECs by enhancing barrier function, reducing inflammation, and restoring metabolic homeostasis. Conclusions This study underscores the pivotal role of the ROS/HIF-1α/GLUT1 axis and demonstrates the therapeutic potential of orientin in UC.
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Advanced Science
·
2026
·
IF 14.1
Tong Yang,Chong Qiu,Yulei Li,Ying Zhang,Chen Wang,Jie Zhou,Zheng Chu,Ang Ma,Ling Huang,Yin Kwan Wong,Junzhe Zhang,Peng Gao,Cui Liu,Junhua Zhang,Huan Tang,Jigang Wang
Triple-negative breast cancer (TNBC) is an aggressive subtype lacking targeted therapies due to the absence of hormone receptors and HER2 expression, resulting in poor clinical outcomes and limited treatment options. Identifying novel vulnerabilities is therefore critical to advancing TNBC therapeutics. Mitochondrial metabolism has emerged as a key regulator of cancer cell survival and proliferation, with serine hydroxymethyltransferase 2 (SHMT2) playing a central role in mitochondrial one-carbon metabolism by supplying one-carbon units for nucleotide biosynthesis and maintaining redox homeostasis. Despite its established importance in cancer metabolism, the functional role and therapeutic potential of SHMT2 in TNBC remain underexplored. Here, we demonstrate that gambogic acid (GA), a natural product with reported anticancer properties, exerts potent and selective cytotoxicity against TNBC cells by covalently targeting SHMT2. GA binds specifically to the critical cysteine residue Cys241, inhibiting SHMT2 enzymatic activity and disrupting mitochondrial function. This leads to bioenergetic collapse, activation of the Nrf2/HO-1 axis, iron overload, and induction of ferroptosis, a non-apoptotic form of cell death increasingly recognized for its therapeutic potential. Our integrative chemoproteomic and mechanistic studies reveal a novel SHMT2-mitochondria-Nrf2/HO-1-ferroptosis axis driving GA's anti-TNBC activity. Moreover, SHMT2 overexpression in TNBC correlates with tumor aggressiveness and poor prognosis, underscoring its role as a metabolic oncogene and promising drug target. These findings establish GA as a novel covalent SHMT2 inhibitor and provide a new framework for exploiting metabolic vulnerabilities to overcome TNBC treatment resistance.
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CHEMICO-BIOLOGICAL INTERACTIONS
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2026
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IF 5.2
Jiaqi Li,Haoyu Chen,Zhengxin Lu,Yuanbiao Ma,Shanshan Li,Zhiyu Chen,Zhewen Deng,Qi Zhang,Bo Ma
Pristimerin (Pri), a natural triterpenoid from the Celastraceae family, exhibits potent anti-tumor and anti-inflammatory activities, yet its further development as a drug candidate is hampered by severe male reproductive toxicity and precise target cells and underlying mechanisms remain unclear. Therefore, this study aimed to identify the target cells and elucidate these mechanisms. In vivo , male mice were administered Pri to evaluate testicular injury, sperm quality, and BTB integrity, while LC-MS/MS was used to detect Pri distribution in testis, epididymis, and sperm, as well as its cellular uptake. In vitro , CCK-8 assessed cell viability, and inhibitor interventions identified contributions of distinct cell death pathways. Annexin V/PI, C11-BODIPY, and DCFH-DA/DHE were used to assess apoptosis and ferroptosis-related oxidative damage. Transcriptomics, RT-qPCR, Western blotting, and immunohistochemistry were performed to examine activation of the NUR77-ATF3-CHOP axis and molecular docking, MD simulations, CETSA, and siRNA-mediated knockdown validated direct NUR77 binding by Pri. Pri exposure induced testicular atrophy, BTB disruption, and sperm impairment, with accumulation in reproductive tissues. In vitro , Pri inhibited TM4 cell viability. Cell death was partially rescued by Z-VAD-FMK and Fer-1, indicating that Pri triggers apoptosis and ferroptosis. Mechanistically, Pri activated the NUR77-ATF3-CHOP axis and directly bound to NUR77, as confirmed by docking, MD simulations, and CETSA. Knockdown of NUR77 improved cell viability and suppressed Pri-induced ATF3 upregulation. Collectively, this study demonstrates that Pri directly targets NUR77, activating the NUR77-ATF3-CHOP axis and inducing both apoptosis and ferroptosis in Sertoli cells, leading to spermatogenesis dysfunction, thereby providing critical insights into Pri-induced testicular injury.
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Frontiers in Cell and Developmental Biology
·
2026
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IF 5.3
Xiaoying Chen,Guanyi Zheng,Kailong Fu,Minglong Yao,Kan Lin
Objective This study was designed to elucidate the molecular pathways responsible for anti-atherosclerotic effects of the traditional Chinese medicine formula Yishen Huoxue Huatan, with a focus on its key active component sesamin. Methods Network pharmacology was applied to predict potential targets and pathways associated with the anti-atherosclerotic activity of Yishen Huoxue Huatan. An atherosclerosis model was constructed in ApoE −/− mice treated with sesamin (50 or 100 mg/kg), and endothelial injury was induced in human umbilical vein endothelial cells (HUVECs) using oxidized low-density lipoprotein (ox-LDL). Aortic pathology, lipid profiles, m 6 A RNA methylation levels, iron accumulation, oxidative stress, and ferroptosis-related markers were assessed. Ferrostatin-1 (Fer-1) was used to verify the involvement of ferroptosis in sesamin-mediated endothelial protection. The involvement of the METTL3/SREBF1 axis was further investigated using RT–qPCR, MeRIP–qPCR, mRNA stability assays, and gene-silencing approaches. Results Network pharmacology identified sesamin as a major bioactive constituent associated with atherosclerosis-related and epigenetic regulatory pathways. In ApoE −/− mice, sesamin reduced aortic lipid deposition, alleviated vascular injury, and improved dyslipidemia. In HUVECs, sesamin attenuated ox-LDL–induced endothelial injury, iron overload, lipid peroxidation, and oxidative stress. Fer-1 produced protective effects similar to those of sesamin, supporting the involvement of ferroptosis inhibition in sesamin-mediated endothelial protection. Mechanistically, sesamin downregulated METTL3 expression and reduced m 6 A modification of SREBF1 mRNA, thereby increasing SREBF1 mRNA stability and protein expression. SREBF1 silencing markedly weakened the anti-ferroptotic effects of sesamin, whereas concurrent METTL3 knockdown partially restored this protective phenotype. Conclusion Sesamin upregulates SREBF1 expression by inhibiting METTL3-mediated m 6 A methylation, thereby alleviating ferroptosis-related alterations in vascular endothelial cells and ultimately delaying the progression of atherosclerosis.
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