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ferroptosis mediated inhibition of breast cancer cells by (3-elemene incorporated GSH/pH dual responsive nanomicelles

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EUROPEAN POLYMER JOURNAL 2025年 223卷

作者： Shen, Sihan Xie, Ran Wang, Yiqun Jia, Lingyu Zhu, Zhangran Ma, Hai Wang, Lifang Sui, Feng Zhao, Yu Zhao, Qinghe Chen, Yanjun China Acad Chinese Med Sci Inst Chinese Mat Med Beijing 100700 Peoples R China

ferroptosis represents a novel procedure of programmed cell death driven by iron-dependent lipid peroxidation, and may offer a promising strategy for cancer therapy. In this study, we developed poly (2-ethyl-2-oxazoline)poly (lactic acid)-SS-poly ((3-amino ester) (PEOz-PLA-SS-PBAE) loaded with (3-elemene. The disulfide bond mediated depletion of glutathione (GSH) and inactivation of glutathione peroxidase 4 (GPX4) will lead to inactivation of the antioxidant system of the tumor cell, and (3-elemene has the capacity to generate reactive oxygen species (ROS), and the above changes would induce a disruption of the redox balance within the tumor cell, resulting in ferroptosis of the tumor cell. In conclusion, in this study, water insoluble (3-elemene was solubilized by the triblock copolymer to construct a pH/GSH dual-responsive nano-delivery system, and combined with iron death and chemotherapy to exert combinatory inhibition effect on breast cancer cells, which provides a new idea for the potential clinical application of (3-elemene.

关键词： ferroptosis (3-elemene Breast cancer pH and GSH dual-responsive

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ferroptosis contributes to immunosuppression

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Frontiers of Medicine 2025年第1期19卷 1-22页

作者： Nina He Dun Yuan Minjie Luo Qing Xu Zhongchi Wen Ziqin Wang Jie Zhao Ying Liu Department of Neurosurgery Xiangya HospitalCentral South UniversityChangsha410008China Department of Pathophysiology Xiangya School of MedicineCentral South UniversityChangsha410008China Sepsis Translational Medicine Key Lab of Hunan Province Changsha410008China National Medicine Functional Experimental Teaching Center Changsha410008China

As a novel form of cell death,ferroptosis is mainly regulated by the accumulation of soluble iron ions in the cytoplasm and the production of lipid peroxides and is closely associated with several diseases,including acute kidney injury,ischemic reperfusion injury,neurodegenerative diseases,and *** term“immunosuppression”refers to various factors that can directly harm immune cells’structure and function and affect the synthesis,release,and biological activity of immune molecules,leading to the insufficient response of the immune system to antigen production,failure to successfully resist the invasion of foreign pathogens,and even organ damage and metabolic *** immunosuppressive phase commonly occurs in the progression of many ferroptosis-related diseases,and ferroptosis can directly inhibit immune cell ***,the relationship between ferroptosis and immunosuppression has not yet been published due to their complicated interactions in various ***,this review deeply discusses the contribution of ferroptosis to immunosuppression in specific *** addition to offering new therapeutic targets for ferroptosis-related diseases,the findings will help clarify the issues on how ferroptosis contributes to immunosuppression.

关键词： ferroptosis immunosuppression immune cells

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ferroptosis: A New Strategy for the Treatment of Fibrotic Diseases

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ADVANCED BIOLOGY 2025年第3期9卷 e2400383页

作者： Pei, Zhuo Fan, Jing Tang, Maolin Li, Yuhong Air Force Hosp Cent Theater Command PLA Datong 037006 Peoples R China Air Force Hosp Northern Theater Command Peoples Li Shenyang 110044 Peoples R China Army Med Univ Dept Cell Biol Chongqing 400038 Peoples R China

ferroptosis is a new type of cell death characterized by iron dependence and the excessive accumulation of lipid reactive oxygen species (lipid ROS) that has gradually become better characterized. There is sufficient evidence indicating that ferroptosis is associated with a variety of human life activities and diseases, such as tumor suppression, ischemic organ injury, and degenerative disorders. Notably, ferroptosis is also involved in the initiation and development of fibrosis in various organs, including liver fibrosis, pulmonary fibrosis, renal fibrosis, and cardiac fibrosis, which is usually irreversible and refractory. Although a large number of patients with fibrosis urgently need to be treated, the current treatment options are still limited and unsatisfactory. Organ fibrosis involves a series of complex and orderly processes, such as parenchymal cell damage, recruitment of inflammatory cells and activation of fibroblasts, which ultimately leads to the accumulation of extracellular matrix (ECM) and the formation of fibrosis. An increasing number of studies have confirmed the close association between these pathological processes and ferroptosis. This review summarizes the role and function of ferroptosis in fibrosis and proposes several potential therapeutic strategies and pathways based on ferroptosis.

关键词： ferroptosis fibrosis Iron treatment

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ferroptosis in space: How microgravity alters iron homeostasis

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ACTA ASTRONAUTICA 2025年 229卷 512-522页

作者： Sivasubramanian, Nithyasree Mumbrekar, Kamalesh Dattaram Prabhu, Sudharshan Manipal Acad Higher Educ Manipal Sch Life Sci Manipal 576104 India Manipal Acad Higher Educ Manipal Sch Life Sci Dept Radiat Biol & Toxicol Manipal 576104 India Manipal Acad Higher Educ Manipal Sch Life Sci Dept Cell & Mol Biol Manipal 576104 Karnataka India

As humanity ventures into space, understanding the effects of microgravity on fundamental cellular, molecular, and physiological processes is essential. Research in this area not only addresses the challenges faced during space exploration but also has the potential to lead to novel discoveries. Microgravity research in the field of biological sciences has gained significant importance as astronauts, cosmonauts, and taikonauts experience various pathological conditions while living under gravity levels vastly different from that on Earth. This review explores insights drawn from space missions and ground-based microgravity simulation models, highlighting changes in iron utilization, storage, transport, recycling, redox signaling, and oxidative stress under microgravity conditions. We aim to elucidate how these alterations may influence the risk of ferroptosis either by exacerbating or mitigating it during space missions. By investigating the effects of microgravity, we gain a deeper understanding of the role of iron and other contributing factors in ferroptotic cell death in space environments. This comprehensive review, therefore, examines the complex interplay between microgravity and iron dynamics, with particular focus on its implication for ferroptosis.

关键词： Microgravity Astronauts Spaceflight Microgravity simulators Astrobiology ferroptosis Iron homeostasis Iron accumulation Oxidative stress

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MOLECULAR NEUROBIOLOGY 2025年第2期62卷 1998-2011页

作者： Li, Xueying Wu, Lei Sun, Linlin Liu, Han Qiao, Xuezhu Mi, Na Yan, Shi Zhang, Xinyu Wang, Kun Quan, Pusheng Yang, Fan Yao, Lifen Harbin Med Univ Affiliated Hosp 1 Dept Neurol Harbin 150081 Peoples R China Chifeng Municipal Hosp Dept Neurol Chifeng 024000 Inner Mongolia Peoples R China Inner Mongolia Med Univ Dept Neurol Affiliated Hosp Hohhot Inner Mongolia Peoples R China

Epilepsy is characterized by a multifaceted aetiology. ferroptosis has recently been implicated in seizure pathophysiology, although its mechanistic role in epilepsy remains obscure. We examined the roles of ferroptosis-related genes (FRGs) in epilepsy cohorts from the GSE143272 dataset. We investigated the associations between gene expression and the immune response by performing CIBERSORT and MCP-counter analyses. By employing unsupervised consensus clustering and weighted gene coexpression network analysis (WGCNA), we delineated robust gene clusters across cohorts. Single-cell RNA sequencing data from the GSE201048 dataset provided insights into the interactions between pivotal ferroptosis-related genes and immune cells. Additionally, we employed qRTPCR technology to measure the levels of these central genes in the tissues of epileptic patients and mice. Our findings revealed seven pivotal genes (TFRC, POR, PTGS2, RELA, PGD, TRIM21, and QSOX1) at the forefront in epilepsy specimens. A diagnostic model harnessing these genes exhibited substantial efficacy (AUC=0.913). Similarly, the qRTPCR analysis of samples from epileptic patients and mouse epileptic brain tissues substantiated these findings. Stratification of 91 patients with epilepsy via WGCNA, based on gene expression, revealed distinct immunological profiles. The scRNA-seq data further indicated increased expression of central genes in macrophages and microglia. Notably, these cells and those with elevated ferroptosis scores were significantly enriched in inflammation-related pathways. These findings support the strong involvement of FRGs in the pathogenesis of epilepsy, particularly neuroinflammation. These central genes hold promise as novel diagnostic biomarkers for epilepsy.

关键词： Epilepsy ferroptosis Single-cell RNA sequencing Immune

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ferroptosis in immune chaos: Unraveling its impact on disease and therapeutic potential

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JOURNAL OF PHYSIOLOGY AND BIOCHEMISTRY 2025年 1-24页

作者： Direksunthorn, Thanyaporn T. Ahmed, Abdulrahman Pluetrattanabha, Nakaraj Uthirapathy, Subasini Ballal, Suhas Singh, Abhayveer Al-Hetty, Hussein Riyadh Abdul Kareem Devi, Anita Sharma, Girish Chandra Yumashev, Alexey Walailak Univ Sch Med Nakhon Si Thammarat Thailand Univ Al Maarif Coll Nursing Al Anbar 31001 Iraq Surat Skin Hair Nails Clin Surat Thani Thailand Tishk Int Univ Pharm Dept Erbil Kurdistan Regio Iraq JAIN Deemed Be Univ Sch Sci Dept Chem & Biochem Bangalore Karnataka India Chitkara Univ Chitkara Univ Inst Engn & Technol Ctr Res Impact & Outcome Rajpura 140401 Punjab India Univ Anbar Coll Educ Pure Sci Dept Biol Ramadi 31001 Anbar Iraq Chandigarh Grp Coll Jhanjeri Chandigarh Engn Coll Dept Appl Sci Mohali 140307 Punjab India NIMS Univ Rajasthan NIMS Inst Engn & Technol Dept Appl Sci Chem Jaipur India Sechenov First Moscow State Med Univ Dept Prosthet Dent Moscow Russia

Since its introduction in 2012, ferroptosis has garnered significant attention from researchers over the past decade. Unlike autophagy and apoptosis, ferroptosis is an atypical iron-dependent programmed cell death that falls under necrosis. It is regulated by various cellular metabolic and signaling processes, which encompass amino acid, lipid, iron, and mitochondrial metabolism. The initiation of ferroptosis occurs through iron-dependent phospholipid peroxidation. Notably, ferroptosis exhibits a dual effect and is associated with various diseases. A significant challenge lies in managing autoimmune disorders with unknown origins that stem from the reactivation of the immune system. Two contributing factors to autoimmunity are the aberrant stimulation of cell death and the inadequate clearance of dead cells, which can expose or release intracellular components that activate the immune response. ferroptosis is distinct from other forms of cell death, such as apoptosis, necroptosis, autophagy, and pyroptosis, due to its unique morphological, biochemical, and genetic characteristics and specific relationship with cellular iron levels. Recent studies indicate that immune cells can both induce and undergo ferroptosis. To better understand how ferroptosis influences immune responses and its imbalance in disease, a molecular understanding of the relationship between ferroptosis and immunity is essential. Consequently, further research is needed to develop immunotherapeutics that target ferroptosis. This review primarily focuses on the role of ferroptosis in immune-related disorders.

关键词： ferroptosis Iron Immune System Autoimmune Diseases

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ferroptosis role in complexity of cell death: unrevealing mechanisms in Parkinson's disease and therapeutic approaches

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INFLAMMOPHARMACOLOGY 2025年第3期33卷 1271-1287页

作者： Awasthi, Anupam Maparu, Kousik Singh, Shamsher ISF Coll Pharm Dept Pharmacol Neuropharmacol Div Moga 142001 Punjab India

Parkinson's disease (PD), a common neurodegenerative disorder, is characterized by progressive loss of dopaminergic neurons, and accumulation of alpha-synuclein in the substantial nigra. Emerging evidence identifies ferroptosis as a regulated iron-dependent cell death mechanism marked by excessive lipid peroxidation (LPO) as a key contributor to PD pathogenesis. ferroptosis is intertwined with critical disease processes such as aggregation of alpha-synuclein protein, oxidative stress generation, mitochondrial alteration, iron homeostasis dysregulation, and neuroinflammation. This mechanism disrupts cellular homeostasis by impairing iron metabolism and antioxidant pathways like the xc-/glutathione/GPX4 axis and the CoQ10 pathway. This review consolidates current advancements in understanding ferroptosis in these mechanisms, increasing interest in contribution to PD pathology. In addition, it explores the latest developments in ferroptosis-targeting pharmacological agents, including their application in the preclinical and clinical study, and highlights their potential to revolutionize PD management. Unraveling the interplay between ferroptosis and PD offers a transformative perspective, paving the way for innovative therapies to combat this debilitating disease condition.

关键词： Parkinson's disease (PD) ferroptosis alpha-Synuclein Neuroinflammation Iron dysregulation Fenton reaction Lipid peroxidation (LPO)

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ferroptosis in Osteoarthritis: Towards Novel Therapeutic Strategy

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CELL PROLIFERATION 2025年第3期58卷 e13779页

作者： Zhang, Yiming Li, Jing Liu, Jiane Gao, Yan Li, Kehan Zhao, Xinyu Liu, Yufeng Wang, Daijie Hu, Xiao Wang, Zheng Qingdao Univ Sch Basic Med Dept Genet & Cell Biol Qingdao Peoples R China Qingdao Univ Affiliated Hosp Dept Reprod Med Qingdao Peoples R China Rizhao Peoples Hosp Dept Hematol Rizhao Peoples R China Qingdao Univ Affiliated Hosp Dept Hematol Qingdao Peoples R China Qilu Univ Technol Shandong Acad Sci Biol Engn Technol Innovat Ctr Shandong Prov Int Joint Lab Med Food R&D & Hlth Prod CreatHeze Heze Peoples R China Chinese Acad Med Sci & Peking Union Med Coll Inst Dermatol Key Lab Basic & Translat Res Immune Mediated Skin Nanjing Peoples R China Chinese Acad Med Sci & Peking Union Med Coll Inst Dermatol Jiangsu Key Lab Mol Biol Skin Dis & STIs Nanjing Peoples R China

Osteoarthritis (OA) is a chronic, degenerative joint disease primarily characterised by damage to the articular cartilage, synovitis and persistent pain, and has become one of the most common diseases worldwide. In OA cartilage, various forms of cell death have been identified, including apoptosis, necroptosis and autophagic cell death. Ever-growing observations indicate that ferroptosis, a newly-discovered iron-dependent form of regulated cell death, is detrimental to OA occurrence and progression. In this review, we first analyse the pathogenetic mechanisms of OA by which iron overload, inflammatory response and mechanical stress contribute to ferroptosis. We then discuss how ferroptosis exacerbates OA progression, focusing on its impact on chondrocyte viability, synoviocyte populations and extracellular matrix integrity. Finally, we highlight several potential therapeutic strategies targeting ferroptosis that could be explored for the treatment of OA.

关键词： ferroptosis mechanism osteoarthritis therapeutic strategy

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ferroptosis in the Substantia Nigra Pars Compacta of Mice: Triggering Role of Ultrafine Diesel Exhaust Particles and Mitigation by α-Lipoic Acid

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NEUROCHEMICAL RESEARCH 2025年第1期50卷 1-13页

作者： Kim, Ji Young Kim, Aryun Kim, Jin-Hee Gil, Young-Chun Kim, Yong-Dae Shin, Dong-Ick Seo, Je Hoon Chungbuk Natl Univ Coll Med Dept Anat Chungdae Ro 1 Cheongju 28644 Chungbuk South Korea Chungbuk Natl Univ Chungbuk Natl Univ Hosp Coll Med Dept Neurosurg Cheongju 28644 Chungbuk South Korea Cheongju Univ Coll Hlth Sci Dept Biomed Lab Sci Cheongju 28503 Chungbuk South Korea Chungbuk Natl Univ Coll Med Dept Prevent Med Cheongju 28644 Chungbuk South Korea Chungbuk Natl Univ Hosp Biomed Res Inst Cheongju 28644 Chungbuk South Korea Chungbuk Natl Univ Hosp Chungbuk Reg Canc Ctr Cheongju 28644 Chungbuk South Korea Chungbuk Natl Univ Hosp Chungbuk Environm Hlth Ctr Cheongju 28644 Chungbuk South Korea

Recent epidemiological and experimental studies have increasingly highlighted the association between environmental pollution, especially ultrafine particulate matter (PM), and the risk of neurodegenerative diseases, such as Parkinson's disease (PD). These previous studies suggest a potential mechanism by which ultrafine PM contributes to neuronal damage through processes, such as iron accumulation and oxidative stress. In this study, we aimed to elucidate the effects of ultrafine PM on ferroptosis, an iron-dependent form of cell death, in the mouse substantia nigra pars compacta (SNc) and to evaluate the protective role of alpha-lipoic acid (ALA). Mice were exposed to ultrafine diesel exhaust particles (ufDEP), a type of ultrafine PM, intranasally and injected ALA intraperitoneally for seven consecutive days. Iron accumulation and lipid peroxidation were significantly increased, and antioxidant capacity was significantly decreased in the SNc after ufDEP exposure, highlighting the deleterious effects of ufDEP on tyrosine hydroxylase (TH)-positive neurons. In contrast, ALA treatment effectively mitigated these effects by reducing iron accumulation, decreasing lipid peroxidation, and restoring antioxidant levels, resulting in the protection of TH-positive neurons from ferroptotic damage. Our results provide evidence that ufDEP can induce ferroptosis in dopaminergic neurons in the SNc, potentially contributing to PD pathogenesis. Furthermore, ALA showed protective effects against ufDEP-induced ferroptotic damage, suggesting its potential as a therapeutic intervention for PD.

关键词： Parkinson's disease ferroptosis Ultrafine diesel exhaust particles alpha-lipoic acid Neuroprotection

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ferroptosis contributed to endoplasmic reticulum stress in preterm birth by targeting LHX1 and IRE-1

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CELLULAR SIGNALLING 2025年 132卷 111777页

作者： Qiu, Liyin Liu, Hui Chen, Shali Wu, Yiting Yan, Jianying Fujian Med Univ Fujian Matern & Child Hlth Hosp Coll Clin Med Obstet & Gynecol & Pediat Dept Obstet 18 Daoshan Rd Fuzhou 350001 Fujian Peoples R China Fujian Med Univ Dept Histol & Embryol Fuzhou Fujian Peoples R China

Preterm birth (PTB) significantly contributed to neonatal mortality, emphasizing the need for a detailed understanding of its pathogenesis. This study aimed to explore the involvement of ferroptosis, an iron-dependent cell death process, in PTB and investigated the possible crosstalk with endoplasmic reticulum stress (ERS). First, we explored the occurrence of ferroptosis in placenta samples from PTB parturients. Then we established a ferroptosis cell model was established by subjecting trophoblast cells to hypoxia/reoxygenation (H/R), and found the ERS was induced in H/R exposed cells and was attenuated by ferroptosis inhibition using Fer-1, suggesting that ferroptosis could induce ERS. Meanwhile, we also induced ERS in trophoblast cells via tunicamycin (TM) treatment. ferroptosis inhibition with Fer-1 alleviated TM-induced ER stress. TM treatment reduced trophoblast cell viability and migration while promoted apoptosis and autophagy, effects that were reversed by ferroptosis inhibition. Thus, targeting ferroptosis might help mitigate ER stress-related pathophysiological changes in PTB. Mechanically, we found two ERS mediators LIM homeobox 1 (LHX1)/Inositol-requiring enzyme 1 (IRE-1) were also upregulated in H/R treated cells. Silencing LHX1 or IRE-1 was demonstrated to reverse the H/R-induced ferroptosis. Additionally, rescue assays further revealed that LHX1 promoted ferroptosis by regulating IRE-1. In conclusion, ferroptosis contributed to ERS and was critically involved in PTB, highlighting the LHX1/IRE-1 axis as a promising therapeutic target for mitigating ferroptosis-related complications. These findings offered a foundation for innovative interventions in preterm birth.

关键词： Preterm birth LHX1 IRE-1 ferroptosis Autophagy Endoplasmic reticulum stress

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