[{"data":1,"prerenderedAt":-1},["ShallowReactive",2],{"detail-sidebar-cat-0-en-105":3,"doc-seo-355476-105":59,"doc-detail-355476-en":131},{"code":4,"msg":5,"data":6},0,"success",[7,13,18,23,28,33,38,43,48,51,55],{"id":8,"doc_module":4,"doc_module_name":9,"category_name":10,"show_sort_weight":11,"slug":12},1,"Document","Story & Novel",90,"story-novel",{"id":14,"doc_module":4,"doc_module_name":9,"category_name":15,"show_sort_weight":16,"slug":17},2,"Literature",80,"literature",{"id":19,"doc_module":4,"doc_module_name":9,"category_name":20,"show_sort_weight":21,"slug":22},4,"Exam",70,"exam",{"id":24,"doc_module":4,"doc_module_name":9,"category_name":25,"show_sort_weight":26,"slug":27},5,"Comic",60,"comic",{"id":29,"doc_module":4,"doc_module_name":9,"category_name":30,"show_sort_weight":31,"slug":32},6,"Technology",50,"technology",{"id":34,"doc_module":4,"doc_module_name":9,"category_name":35,"show_sort_weight":36,"slug":37},7,"Healthcare",40,"healthcare",{"id":39,"doc_module":4,"doc_module_name":9,"category_name":40,"show_sort_weight":41,"slug":42},8,"Research & Report",30,"research-report",{"id":44,"doc_module":4,"doc_module_name":9,"category_name":45,"show_sort_weight":46,"slug":47},9,"Religion & Spirituality",20,"religion-spirituality",{"id":46,"doc_module":4,"doc_module_name":9,"category_name":49,"show_sort_weight":46,"slug":50},"World Cup","world-cup",{"id":52,"doc_module":4,"doc_module_name":9,"category_name":53,"show_sort_weight":52,"slug":54},10,"Lifestyle","lifestyle",{"id":56,"doc_module":4,"doc_module_name":9,"category_name":57,"show_sort_weight":24,"slug":58},19,"General","general",{"code":4,"msg":60,"data":61},"ok",{"site_id":62,"language":63,"slug":64,"title":65,"keywords":66,"description":67,"schema_data":68,"social_meta":124,"head_meta":126,"extra_data":128,"updated_unix":130},105,"en","ginsenoside-mediated-ferroptosis-regulation-bidirectional-effects-and-therapeutic-potential-in-diseases","Ginsenoside-Mediated Ferroptosis Regulation - Bidirectional Effects and Therapeutic Potential in Diseases","","Certain ginsenoside components show disease-context-dependent, bidirectional regulation of ferroptosis. In aberrantly proliferating or activated cells, ginsenosides act as ferroptosis inducers by modulating iron metabolism proteins and weakening antioxidant defenses such as GPX4 and SLC7A11, driving iron overload and lipid peroxidation that culminate in ferroptosis. In damaged quiescent cells of normal tissues, they function as inhibitors by maintaining iron homeostasis via upregulating FTH1, downregulating TFRC, and limiting labile Fe2+ accumulation, thereby blocking ferroptosis initiation.",{"@graph":69,"@context":123},[70,84,106],{"@type":71,"itemListElement":72},"BreadcrumbList",[73,77,79,82],{"item":74,"name":75,"@type":76,"position":8},"https://docshare.wps.com","Home","ListItem",{"item":78,"name":9,"@type":76,"position":14},"https://docshare.wps.com/document/",{"item":80,"name":35,"@type":76,"position":81},"https://docshare.wps.com/document/healthcare/",3,{"item":83,"name":65,"@type":76,"position":19},"https://docshare.wps.com/document/ginsenoside-mediated-ferroptosis-regulation-bidirectional-effects-and-therapeutic-potential-in-diseases/355476/",{"url":83,"name":65,"@type":85,"image":86,"author":91,"headline":65,"publisher":94,"fileFormat":97,"inLanguage":63,"description":67,"dateModified":98,"datePublished":99,"encodingFormat":97,"isAccessibleForFree":100,"interactionStatistic":101},"DigitalDocument",{"url":87,"@type":88,"width":89,"height":90},"https://docshare.wps.com/thumbnails/ginsenoside-mediated-ferroptosis-regulation-bidirectional-effects-and-therapeutic-potential-in-diseases/355476.png","ImageObject",300,407,{"name":92,"@type":93},"Aria Callaghan","Person",{"url":74,"name":95,"@type":96},"DocShare","Organization","application/pdf","2026-10-30","2026-09-22",true,{"@type":102,"interactionType":103,"userInteractionCount":105},"InteractionCounter",{"@type":104},"ViewAction",16,{"@type":107,"mainEntity":108},"FAQPage",[109,115,119],{"name":110,"@type":111,"acceptedAnswer":112},"How do ginsenosides regulate ferroptosis differently across disease contexts?","Question",{"text":113,"@type":114},"Ginsenosides exhibit bidirectional effects: they induce ferroptosis in aberrantly proliferating/activated cells but inhibit ferroptosis in damaged, non-proliferative cells under pathological insults.","Answer",{"name":116,"@type":111,"acceptedAnswer":117},"What mechanisms underlie the pro-ferroptotic action of ginsenosides?",{"text":118,"@type":114},"They modulate iron metabolism proteins and suppress antioxidant defense systems, such as GPX4 and SLC7A11, leading to iron overload and extensive lipid peroxidation that trigger ferroptosis.",{"name":120,"@type":111,"acceptedAnswer":121},"What mechanisms support the anti-ferroptotic effects in normal tissues?",{"text":122,"@type":114},"They help maintain iron homeostasis by upregulating iron storage proteins like FTH1, downregulating iron uptake proteins such as TFRC, and inhibiting labile Fe2+ accumulation to prevent ferroptosis initiation.","https://schema.org",{"og:url":83,"og:type":125,"og:title":65,"og:site_name":95,"og:description":67},"article",{"robots":127,"canonical":83},"index,follow",{"doc_id":129,"site_id":62},355476,1790337739,{"code":4,"msg":5,"data":132},{"doc_id":129,"user_id":133,"nickname":92,"user_avatar":134,"doc_module":4,"category_id":34,"category_name":35,"doc_title":65,"doc_description":67,"doc_content":135,"file_id":136,"file_url":137,"file_type":138,"file_size":139,"view_count":105,"is_deleted":4,"is_public":8,"is_downloadable":8,"audit_status":8,"page_count":140,"language":141,"language_code":63,"site_id":62,"html_lang":63,"table_of_contents":142,"faqs":143,"seo_title":144,"seo_description":67,"update_tm":145,"read_time":146},962084926284,"https://ap-avatar.wpscdn.com/davatar_29158cc5080c5b710cf443261637dec0","Review  \nGinsenoside-Mediated Ferroptosis Regulation: Bidirectional Effects and Therapeutic Potential in Diseases  \nYuanyuan Wang 1, Mengxue Song 2, Shuai Li 1, Huizhen Ren 1, Shuang Liu 1,* and Hui Zhang 1, *  \nReceived: 12 January 2026  \nRevised: 23 February 2026  \nAccepted: 27 February 2026  \nPublished: 31 March 2026  \nCopyright: © 2026 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license.  \n1 School of Basic Medicine, Jiamusi University, Jiamusi 154007, China; [wyuanyuan202303@163.com](wyuanyuan202303@163.com) (Y.W.); [15686061872@163.com](15686061872@163.com) (S.L.); [18735054637@163.com](18735054637@163.com) (H.R.)  \n2 School of Clinical Medicine, Jiamusi University, Jiamusi 154007, China; [18212685516@163.com](18212685516@163.com)  \n* Correspondence: [lius@jmsu.edu.cn](lius@jmsu.edu.cn) (S.L.); [zhanghui@jmsu.edu.cn](zhanghui@jmsu.edu.cn) (H.Z.)  \nAbstract  \nNotably, certain ginsenoside components exhibit distinct bidirectional and contextdependent regulatory effects on ferroptosis depending on the disease setting. In aberrantly proliferating or activated cells, ginsenosides function as ferroptosis inducers, whereas in damaged quiescent cells of normal tissues, they act as ferroptosis inhibitors. The proferroptotic effect is predominantly observed in cells characterized by abnormal proliferation or activation, such as cancer cells and activated hepatic stellate cells in liver fibrosis. In this context, ginsenosides modulate key iron metabolism proteins and suppress antioxidant defense systems (e.g., GPX4, SLC7A11), thereby triggering intracellular iron overload and explosive lipid peroxidation, ultimately culminating in ferroptosis. Conversely, the anti-ferroptotic effect primarily targets damaged non-proliferative cells in normal tissues subjected to pathological insults (e.g., ischemia–reperfusion, inflammation) . In this setting, the regulatory focus of ginsenosides shifts toward maintaining iron homeostasis through mechanisms including upregulation of iron storage proteins (e.g., FTH1), downregulation of iron uptake proteins (e.g., TFRC), and inhibition of labile Fe2+ accumulation, thereby blocking ferroptosis initiation. This review systematically elucidates the pharmacological effects and underlying mechanisms by which different ginsenoside components regulate ferroptosis across various disease contexts and cell types, with particular emphasis on their disease-and cell type-dependent bidirectional regulatory characteristics. By highlighting these context-specific effects, we aim to provide novel potential therapeutic targets and mechanistic insights for the precision treatment of diverse pathological conditions, including malignant proliferative disorders, non-malignant aberrantly activated/proliferative diseases such as liver fibrosis, and cell injury/degenerative diseases.  \nKeywords: ginseng; ginsenoside; ferroptosis; cancer; non-cancer disease  \n1. Introduction  \nIn recent years, Traditional Chinese medicine (TCM) has attracted extensive research attention due to its broad spectrum of pharmacological activities, remarkable therapeutic efficacy, and favorable safety profile. Beyond multi-herb compound prescriptions, TCM also includes diverse individual active components. These exhibit remarkable chemical structural diversity and demonstrate extensive biological activities [1] . Previous studies have shown that several traditional Chinese medicines can effectively inhibit the proliferation of tumor cells by regulating cell death mechanisms such as pyroptosis and apoptosis [2] .  \nNotably, accumulating evidence suggests that some TCMs can further influence the development of diverse diseases through the modulation of ferroptosis [3], and ginseng stands out as a prominent representative among such natural medicinal materials. Regarded asa precious medicinal herb in TCM, ginseng exhibi","cbCaie0SUbBeJe8d","https://ap.wps.com/l/cbCaie0SUbBeJe8d","pdf",3067137,33,"English","# Introduction\n## Traditional Chinese medicine and ginseng background\n## Ginsenosides as active components and their anti-disease effects\n## Ferroptosis and its role in disease development","[{\"question\":\"How do ginsenosides regulate ferroptosis differently across disease contexts?\",\"answer\":\"Ginsenosides exhibit bidirectional effects: they induce ferroptosis in aberrantly proliferating/activated cells but inhibit ferroptosis in damaged, non-proliferative cells under pathological insults.\"},{\"question\":\"What mechanisms underlie the pro-ferroptotic action of ginsenosides?\",\"answer\":\"They modulate iron metabolism proteins and suppress antioxidant defense systems, such as GPX4 and SLC7A11, leading to iron overload and extensive lipid peroxidation that trigger ferroptosis.\"},{\"question\":\"What mechanisms support the anti-ferroptotic effects in normal tissues?\",\"answer\":\"They help maintain iron homeostasis by upregulating iron storage proteins like FTH1, downregulating iron uptake proteins such as TFRC, and inhibiting labile Fe2+ accumulation to prevent ferroptosis initiation.\"}]","Ginsenoside-Mediated Ferroptosis Regulation - Bidirectional Effects and Therapeutic Potential in Diseases | PDF",1790119254,83]