Apoptosis最新文献

{"title":"HSV-1 hijacks mitochondrial dynamics: potential molecular mechanisms linking viral infection to neurodegenerative disorders","authors":"Siping Kuang,&nbsp;Zhiyang He,&nbsp;Jingjing Zhang,&nbsp;Shuli Li,&nbsp;Juntao Ding,&nbsp;Zhenghai Ma,&nbsp;Beibei Zhang","doi":"10.1007/s10495-025-02142-9","DOIUrl":"10.1007/s10495-025-02142-9","url":null,"abstract":"<div><p>Herpes simplex virus type 1 (HSV-1), a neurotropic virus, hijacks the critical neuronal organelle—mitochondria—to establish lifelong latent infection and potentially accelerate neurodegenerative pathologies. Research indicates that HSV-1 infection disrupts mitochondrial dynamics, impairs its bioenergetic function, and compromises interorganellar communication. This disruption is primarily achieved through the degradation of mitochondrial DNA (mtDNA) and the functional alteration of key proteins, leading to excessive production of reactive oxygen species (ROS), intracellular calcium dysregulation, and abnormal energy metabolism. These alterations not only diminish cellular energy production and exacerbate oxidative damage but also readily trigger neuronal cell death. Crucially, the virus specifically interferes with mitochondrial-endoplasmic reticulum contact sites (MERCs) to evade immune surveillance while simultaneously promoting its own replication. In severe encephalitis, mitochondrial damage is closely associated with neuroinflammation. For Alzheimer's disease (AD), HSV-1 may synergize with amyloid-beta pathology through ROS and viral proteins (such as glycoprotein B (gB) and glycoprotein I (gI)), exacerbating disease progression. Paradoxically, HSV-1 also inhibits immediate cell death to sustain host cell survival, facilitating latent viral reactivation. Research elucidating how the virus exploits mitochondria for pathogenesis suggests that future therapeutic strategies could combine classical antiviral drugs with agents that protect mitochondrial function (e.g., antioxidants). This combined approach holds promise for combating acute infection and potentially mitigating the progression of associated neurodegenerative diseases.</p></div>","PeriodicalId":8062,"journal":{"name":"Apoptosis","volume":"30 9-10","pages":"1913 - 1930"},"PeriodicalIF":8.1,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144537859","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"DNA damage repair inhibitors boost targeted radionuclide therapy and immunotherapy of prostate cancer","authors":"Bin Xu,&nbsp;Lei Tao,&nbsp;Juan Sun,&nbsp;Jiangtao Yang,&nbsp;Fenghua Meng,&nbsp;Zhiyuan Zhong","doi":"10.1007/s10495-025-02136-7","DOIUrl":"10.1007/s10495-025-02136-7","url":null,"abstract":"<div><p>Targeted radionuclide therapy (TRT) has emerged as a valuable treatment for metastatic castration-resistant prostate cancer (mCRPC) patients. The radioresistance coupled with heterogeneity and immunosuppressive tumor microenvironment of mCRPC, however, greatly restricts the clinical response and anticancer immunity. Here, we found that DNA damage repair inhibitors, in particular ATM inhibitor (ATMi), effectively boost TRT and immunotherapy of prostate cancer. ATMi significantly amplified TRT-induced DNA damage and immunogenic cell death in tumor cells, by impairing double-strand break repair and arresting cell cycle progression, which reshaped the tumor microenvironment and markedly improved tumor inhibition and survival rate in murine RM-1-hPSMA tumor model. Intriguingly, addition of αCTLA-4 antibody further resulted in 71% mice complete regression. TRT in combination with ATMi and αCTLA-4 appeared to boost adaptive and long-lasting anticancer immunity. Our results signify that ATM inhibitor not only sensitizes targeted radionuclide therapy but also effectively augments immune checkpoint inhibitor therapy.</p></div>","PeriodicalId":8062,"journal":{"name":"Apoptosis","volume":"30 9-10","pages":"2238 - 2253"},"PeriodicalIF":8.1,"publicationDate":"2025-06-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144493730","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The role of the NcRNA/ferroptosis axis in lung cancer: molecular mechanisms and potential therapeutic targets","authors":"Mina Alimohammadi,&nbsp;Samaneh Kahkesh,&nbsp;William C. Cho,&nbsp;Najma Farahani,&nbsp;Mahdi Farhadi Khoozani,&nbsp;Ahmadreza Zare,&nbsp;Amirreza Nejadheidari,&nbsp;Marzieh Ramezani Farani,&nbsp;Afsaneh Kheirmand Parizi,&nbsp;Fereshteh Asgharzadeh,&nbsp;Seyedeh Mahdieh Khoshnazar,&nbsp;Mehrdad Hashemi,&nbsp;Afshin Taheriazam,&nbsp;Kiavash Hushmandi","doi":"10.1007/s10495-025-02127-8","DOIUrl":"10.1007/s10495-025-02127-8","url":null,"abstract":"<div><p>Lung cancer, the second most diagnosed malignancy globally, remains the leading cause of cancer-related deaths due to its aggressive nature and limited treatment success. Ferroptosis, a unique form of regulated cell death, is characterized by iron-dependent lipid peroxidation and oxidative stress, distinct from apoptosis and necrosis. It plays a dual role in cancer by promoting cell death while being suppressed in tumor progression. This suppression allows cancer cells, including lung cancer cells, to evade destruction, contributing to the disease’s malignancy. However, ferroptosis-inducing agents have shown promise in targeting cancer cells resistant to conventional therapies, positioning ferroptosis as a therapeutic avenue in oncology. Non-coding RNAs (ncRNAs) emerge as pivotal regulators in this axis. These molecules, including microRNAs (miRNAs), long non-coding RNAs (lncRNAs), and circular RNAs (circRNAs), modulate ferroptosis-related pathways by targeting key regulators like GPX4, SLC7A11, and ACSL4. For instance, miRNAs can downregulate SLC7A11, enhancing sensitivity to ferroptosis, while lncRNAs can stabilize or suppress pathways that prevent lipid peroxidation. CircRNAs, acting as molecular sponges, influence ferroptosis by modulating miRNA activity. The deregulation of these ncRNAs in lung cancer underscores their significance in the disease’s pathogenesis and progression. Understanding the ncRNA-ferroptosis axis offers a novel perspective in addressing this challenge. Therapeutic strategies targeting this axis aim to selectively induce ferroptosis in tumor cells while sparing normal cells, enhancing treatment specificity and efficacy. Furthermore, combining ncRNA-based therapeutics with ferroptosis inducers provides a promising framework for overcoming drug resistance and improving outcomes. This review highlights comprehensive insight into the molecular mechanisms and therapeutic potential of the ncRNA-ferroptosis axis that could pave the way for more effective lung cancer treatments.</p><h3>Graphical abstract</h3><div><figure><div><div><picture><source><img></source></picture></div></div></figure></div></div>","PeriodicalId":8062,"journal":{"name":"Apoptosis","volume":"30 7-8","pages":"1665 - 1694"},"PeriodicalIF":8.1,"publicationDate":"2025-06-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144367830","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Acute high-altitude hypoxia induced NLRP3 inflammasome activation in pulmonary artery smooth muscle cells by BMAL1 targeting mitochondrial VDAC1-mediated MtDNA leakage","authors":"Si-Yuan He,&nbsp;Ying-Rui Bu,&nbsp;Jin Xu,&nbsp;Yu-Meng Wang,&nbsp;Tian-Xi Feng,&nbsp;Pei-Jie Li,&nbsp;Yi-Xiao Zhao,&nbsp;Yi-Ling Ge,&nbsp;Man-Jiang Xie","doi":"10.1007/s10495-025-02138-5","DOIUrl":"10.1007/s10495-025-02138-5","url":null,"abstract":"<div><p>Hypoxia-induced inflammatory injury is an important pathological mechanism underlying the progression of acute mountain sickness (AMS). Recent studies reported that molecular clock could control mitochondrial pathways to involve hypoxic and inflammatory responses. Excessively released mitochondrial DNA (mtDNA) acts as a damage-associated molecular pattern (DAMP) to trigger inflammation in many diseases. Herein, we subjected mice at a simulated altitude of 5500 m for 3 days and found that the expression levels of inflammatory cytokines were significantly increased in mouse pulmonary arteries, accompanied by mtDNA release and NLRP3 inflammasome activation in the pulmonary artery smooth muscle cells (PASMCs). RNA-sequencing and loss- and gain-of function experiments indicated that the core clock component BMAL1 regulated mtDNA leakage in PASMCs, and smooth muscle-specific <i>Bmal1</i> knockout significantly alleviated the pulmonary arterial inflammation under acute high-altitude hypoxia. Mechanically, BMAL1 as a transcription factor directly promoted the transcriptional expression of Voltage-dependent anion channel 1 (VDAC1) and exacerbated the VDAC1-mediated mtDNA leakage under hypoxia, which activated NLRP3 inflammasome signaling in PASMCs and induced vascular inflammation. Our work provides mechanistic insights into the hypoxia-induced inflammation in PASMCs and may provide a novel therapeutic approaching for targeting BMAL1-VDAC1 in AMS.</p></div>","PeriodicalId":8062,"journal":{"name":"Apoptosis","volume":"30 9-10","pages":"2225 - 2237"},"PeriodicalIF":8.1,"publicationDate":"2025-06-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144367818","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Zinc ions trigger PANoptosis-like cell death in magnetic hyperthermia therapy of magnesium based implant for hepatocellular carcinoma","authors":"Anhong Liu,&nbsp;Xiao Han,&nbsp;Qianqian Yang,&nbsp;Xiangxue Meng,&nbsp;Hao Qiu,&nbsp;Chunjie Wu,&nbsp;Xiaoming Li,&nbsp;Mengmeng Cai,&nbsp;Tinghe Duan,&nbsp;Zhanhui Wang","doi":"10.1007/s10495-025-02132-x","DOIUrl":"10.1007/s10495-025-02132-x","url":null,"abstract":"<div><p>The treatment of hepatocellular carcinoma (HCC) is a worldwide urgent and pressing challenge. Magnetic hyperthermia therapy (MHT) is a relatively new therapeutic strategy for tumors in resent years, especially magnesium (Mg) implants with eddy thermal effect can be employed for MHT to therapy tumor. PANoptosis is a new type of programmed cell death (PCD), driven by Caspases and RIPKs through the formation of PANoptosomes. In our early study, we discovered Zn²⁺ came from Zn-LDH@Mg implant could induce pyroptosis. In this work, we further demonstrate that Zn²⁺ comes from Zn-LDH@Mg implant can induce PANoptosis-like cell death in MHT to therapy H22 cells and tumors, verified by immunofluorescence staining, TUNEL staining, western blot assay, ELISA and transcriptomics analysis. This work is the first time to combine MHT and PANoptosis to therapy HCC, emphasizing the importance of materials design for MHT, and providing a useful foundation for materials design combined with PCD to treat tumors.</p></div>","PeriodicalId":8062,"journal":{"name":"Apoptosis","volume":"30 7-8","pages":"1826 - 1838"},"PeriodicalIF":8.1,"publicationDate":"2025-06-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144332366","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The CXCL8-CXCR2 axis promotes M2 macrophage polarization in ovarian cancer via RASGRP4-mediated mTOR-STAT3 signaling","authors":"Mi Ren,&nbsp;Ling-ling Chen,&nbsp;Lin-yin Jiang,&nbsp;Hui-hui Yu,&nbsp;Hai-zhou Ji","doi":"10.1007/s10495-025-02128-7","DOIUrl":"10.1007/s10495-025-02128-7","url":null,"abstract":"<div><p>This study aimed to investigate whether CXCL8-CXCR2 axis in regulating M2 macrophage polarization via RASGRP4 related signaling in ovarian cancer. Data from The Cancer Genome Atlas (TCGA) database was used to assess the correlation between CXCR2 expression and M2 macrophage infiltration. THP-1 human monocytic cells were utilized to analyze the effects of CXCL8 on RASGRP4 expression and M2 polarization. In vivo experiments were conducted using xenograft models to evaluate the impact of CXCL8 and RASGRP4 on tumor growth and macrophage polarization. Among the CXCR2 co-expressed genes, <i>RASGRP4</i> showed the highest positive correlation with M2 macrophage infiltration in ovarian cancer. Higher expression of <i>RASGRP4</i> is associated with poorer progression-free survival in patients with serous ovarian cancer. <i>CXCR2</i> knockdown or inhibition (using SB225002) reduced IL-8-induced upregulation of RASGRP4 mRNA and protein in THP-1 cells. Additionally, PLCβ2 silencing attenuated IL-8-induced RASGRP4 expression. Knockdown of <i>RASGRP4</i> in THP-1 cells reduced M2 polarization, while overexpression restored it. The CXCL8-CXCR2 axis further enhances M2 polarization through RASGRP4-mediated mTOR-STAT3 signaling. In xenograft ovarian tumor models, knockdown of <i>CXCL8</i>, <i>CXCR2</i>, or <i>RASGRP4</i> reduced tumor growth and M2 macrophage infiltration. In summary, the CXCL8-CXCR2 axis promotes M2 macrophage polarization via RASGRP4-mediated mTOR-STAT3 signaling in ovarian cancer. Targeting this pathway may be a promising therapeutic strategy to reprogram tumor-associated macrophages and enhance treatment efficacy.</p></div>","PeriodicalId":8062,"journal":{"name":"Apoptosis","volume":"30 7-8","pages":"1839 - 1851"},"PeriodicalIF":8.1,"publicationDate":"2025-06-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144293238","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Silencing IFIT3 suppresses the EGFR/VEGF pathway and modulates SOCS1 to attenuate skin fibrosis in systemic sclerosis","authors":"Xiangyang Huang,&nbsp;Yi Liu,&nbsp;Hangling Fu,&nbsp;Xia Rong,&nbsp;Yiheng Zhao","doi":"10.1007/s10495-025-02115-y","DOIUrl":"10.1007/s10495-025-02115-y","url":null,"abstract":"<div><p>Systemic sclerosis (SSc) is a life-threatening autoimmune disease characterized by progressive skin and organ fibrosis. Although interferon signaling is dysregulated in SSc, the role of interferon-induced proteins like IFIT3 in the skin fibrosis of SSC remains unclear. Here, we demonstrate that IFIT3 expression is significantly elevated (<i>p</i> &lt; 0.01) in SSc fibroblasts and promotes fibrosis via SOCS1-dependent activation of the EGFR/VEGF axis. Silencing IFIT3 upregulated SOCS1 (<i>p</i> &lt; 0.05), suppressed EGFR/VEGF (<i>p</i> &lt; 0.01), and inhibited fibroblast proliferation/migration (<i>p</i> &lt; 0.01). In a bleomycin-induced SSc model, IFIT3 knockdown ameliorated skin/lung collagen deposition and fibrosis (<i>p</i> &lt; 0.05). Our findings reveal a novel mechanism whereby IFIT3 regulates EGFR and VEGF through down-regulating SOCS1 in SSc fibrosis, identifying IFIT3 as a novel therapeutic target for SSc.</p></div>","PeriodicalId":8062,"journal":{"name":"Apoptosis","volume":"30 7-8","pages":"1852 - 1874"},"PeriodicalIF":8.1,"publicationDate":"2025-06-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144293237","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A novel programmed cell death signature predicts clinical outcomes in clear cell renal cell carcinoma and identifies PLK1 as a therapeutic target","authors":"Hao-tian Tan,&nbsp;Chang-yu Ma,&nbsp;Chong-hao Sun,&nbsp;Shu-zhan Sun,&nbsp;Ming-xiao Zhang,&nbsp;Jian-feng Wang","doi":"10.1007/s10495-025-02126-9","DOIUrl":"10.1007/s10495-025-02126-9","url":null,"abstract":"<div><p>Clear-cell renal cell carcinoma (ccRCC) remains therapeutically challenging despite recent treatment advances. Here, we analyzed 18 distinct programmed cell death (PCD) patterns across multiple cohorts and developed a novel prognostic scoring system (PCDscore) based on eight PCD-related genes. We established an eight-gene signature that demonstrated robust predictive capability and, when integrated with clinical staging, yielded a nomogram with strong performance across independent cohorts. High PCDscore groups exhibited enhanced immunosuppressive features, while low PCDscore groups showed better immunotherapy responses. Single-cell analysis of 54,166 cells revealed activation of multiple oncogenic pathways in high PCDscore tumor cells, along with extensive intercellular communication networks. To further investigate the role of PLK1, we identified 282 co-expressed genes and conducted functional enrichment analyses, revealing its significant association with pathways such as the cell cycle and NF-κB signaling. A protein–protein interaction (PPI) network and Bayesian network analysis highlighted PLK1 as a key regulator of PKMYT1, with CDC20 and CCNB2 acting upstream. Functional validation confirmed PLK1, the highest weighted gene in our signature, significantly influences tumor progression in ccRCC. This study establishes a reliable prognostic scoring system and identifies PLK1 as a potential therapeutic target, providing valuable clinical guidance for treatment decision-making in ccRCC patients.</p></div>","PeriodicalId":8062,"journal":{"name":"Apoptosis","volume":"30 7-8","pages":"1797 - 1825"},"PeriodicalIF":8.1,"publicationDate":"2025-06-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144246093","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Ferroptosis: a novel therapeutic warrior in the battle against leukemia","authors":"Yiduo Bai,&nbsp;Yizhi Luo,&nbsp;Yiyi Yuan,&nbsp;Xuan Li,&nbsp;Junchang Jin,&nbsp;Ruijing Ping,&nbsp;Jiuru Guo,&nbsp;Liuxu Jin,&nbsp;Yi Yu,&nbsp;Yuyan Xiong","doi":"10.1007/s10495-025-02130-z","DOIUrl":"10.1007/s10495-025-02130-z","url":null,"abstract":"<div><p>Ferroptosis is a newly discovered form of iron-dependent programmed cell death, characterized by the accumulation of lethal lipid peroxidation (LPO) driven by iron overload and dysregulated intracellular redox homeostasis. Leukemia, a heterogeneous group of malignant blood system tumors, typically manifests with increased oxidative stress and iron overload. A growing body of studies have revealed intimate interactions between ferroptosis and leukemia. Induction of ferroptosis has been demonstrated to mitigate the development and progression of leukemia, thus providing novel insights into potential therapeutic strategies for leukemia. In this review, we examine the characteristics and biological processes of ferroptosis, highlighting the action mechanisms of key ferroptosis-related regulators, including iron, glutathione (GSH), glutathione peroxidase 4 (GPX4), system X_c⁻, lipid reactive oxygen species (ROS), p53, and mitochondria, in contributing to leukemia. This review also underscores the significant therapeutic potential of targeting ferroptosis in leukemia therapy using regulators such as system X_c⁻ inhibitors, GSH/GPX4 inhibitors, lipid ROS inducers, and natural compounds. Finally, we identify key unresolved questions and challenges that warrant further investigation in future translational studies.</p><h3>Graphic abstract</h3><div><figure><div><div><picture><source><img></source></picture></div></div></figure></div></div>","PeriodicalId":8062,"journal":{"name":"Apoptosis","volume":"30 7-8","pages":"1776 - 1795"},"PeriodicalIF":8.1,"publicationDate":"2025-06-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144246095","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A new perspective on iron-dependent cell death: PRDX-1-mediated ferroptosis in tumor cells","authors":"Rui Li,&nbsp;Zhiyuan Wang,&nbsp;Yueyue Yujiang,&nbsp;Mengyuan Hu,&nbsp;Hongkun Zhao,&nbsp;Fei Yan","doi":"10.1007/s10495-025-02129-6","DOIUrl":"10.1007/s10495-025-02129-6","url":null,"abstract":"<div><p>Ferroptosis is a novel regulated cell death characterized by excessive membrane lipid peroxidation in an iron- and ROS-dependent manner, which is increasingly recognized for its role in tumor suppression and overcoming therapy resistance in various cancers. Induction of ferroptosis has been shown to sensitize cancer cells to chemotherapy, targeted therapy, and immunotherapy, thereby providing a novel strategy to tumor therapy. Peroxiredoxin 1 (PRDX1), an antioxidant enzyme, regulates redox homeostasis and is involved in tumor invasion, metastasis and prognosis. Increasing evidence suggests that PRDX1 is a negative regulator of ferroptotic cell death. Hence, regulating ferroptosis, via targeting PRDX1 and regulating PRDX1’ function, holds promise for the treatment of tumors. In this review, we comprehensively summarized the regulatory of PRDX1 on ferroptosis and discussed the potential of PRDX1-mediated ferroptosis on tumor therapy, aiming to provide a distinct method for finding potential targets to enhance the effectiveness of ferroptosis-based tumor treament.</p></div>","PeriodicalId":8062,"journal":{"name":"Apoptosis","volume":"30 7-8","pages":"1645 - 1664"},"PeriodicalIF":8.1,"publicationDate":"2025-06-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144246092","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}