[{"data":1,"prerenderedAt":-1},["ShallowReactive",2],{"detail-sidebar-cat-0-en-105":3,"doc-seo-417734-105":59,"doc-detail-417734-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","galectin-3-in-acute-myocardial-infarction-from-molecular-mechanisms-to-clinical-translation","Galectin-3 in acute myocardial infarction: from molecular mechanisms to clinical translation","","Galectin-3 is a β-galactoside-binding lectin implicated in the pathophysiology following acute myocardial infarction (AMI). This review synthesizes evidence on its molecular functions, biomarker utility, and therapeutic targeting, covering signaling pathways, clinical correlations, and preclinical interventional models. Galectin-3 promotes post-AMI inflammation via NF-κB activation, macrophage polarization, and fibrosis through TGF-β/Smad-related fibroblast activation, while also regulating apoptosis and oxidative/endoplasmic reticulum stress. Clinically, dynamic circulating levels associate with infarct size, adverse ventricular remodeling, major events, and treatment response, supporting inhibition as a promising strategy pending further translation.",{"@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/galectin-3-in-acute-myocardial-infarction-from-molecular-mechanisms-to-clinical-translation/417734/",{"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/galectin-3-in-acute-myocardial-infarction-from-molecular-mechanisms-to-clinical-translation/417734.png","ImageObject",300,407,{"name":92,"@type":93},"Emma Wilson","Person",{"url":74,"name":95,"@type":96},"DocShare","Organization","application/pdf","2026-11-06","2026-09-28",true,{"@type":102,"interactionType":103,"userInteractionCount":105},"InteractionCounter",{"@type":104},"ViewAction",11,{"@type":107,"mainEntity":108},"FAQPage",[109,115,119],{"name":110,"@type":111,"acceptedAnswer":112},"What role does galectin-3 play in AMI after injury?","Question",{"text":113,"@type":114},"Galectin-3 functions as a damage-associated molecular pattern that drives key post-AMI pathologies, including inflammation, fibrosis, and regulation of apoptosis and cellular stress responses.","Answer",{"name":116,"@type":111,"acceptedAnswer":117},"How is galectin-3 useful clinically in acute myocardial infarction?",{"text":118,"@type":114},"Elevated circulating galectin-3 correlates with infarct size, adverse ventricular remodeling, and poor outcomes, and serial measurements may reflect treatment response after PCI or statin therapy.",{"name":120,"@type":111,"acceptedAnswer":121},"What evidence supports galectin-3 as a therapeutic target?",{"text":122,"@type":114},"Preclinical models show that genetic ablation or pharmacological inhibition of galectin-3 attenuates inflammation, fibrosis, and cardiac dysfunction, although clinical translation requires further investigation.","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},417734,1790790626,{"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,"preview_page_count":4},3848291630094,"https://eur-avatar.wpscdn.com/davatar_085a072bc5b1113ac321206ff7593b45","TYPE Review  \nPUBLISHED 19 December 2025 DOI 10.3389/fmolb.2025.1730173  \nOPEN ACCESS  \nEDITED BY  \nEleonora Cianflone,  \nMagna Græcia University, Italy  \nREVIEWED BY  \nGloria Riitano,  \nSapienza University of Rome, Italy Ivica Bosnjak,  \nOsijek Clinical Hospital Center, Croatia  \n*CORRESPONDENCE  \nFang Yang,  \n [3599531282@qq.com](3599531282@qq.com)  \nRECEIVED 31 October 2025  \nREVISED 03 December 2025  \nACCEPTED 04 December 2025  \nPUBLISHED 19 December 2025  \nCITATION  \nLiu T and Yang F (2025) Galectin-3 in acute myocardial infarction: from molecular mechanisms to clinical translation.  \nFront. Mol. Biosci. 12:1730173 .  \ndoi: 10.3389/fmolb.2025.1730173  \nCOPYRIGHT  \n© 2025 Liu and Yang. This is an open-access article distributed under the terms of the  \nCreative Commons Attribution License (CC BY) . The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.  \nGalectin-3 in acute myocardial infarction: from molecular mechanisms to clinical translation  \nTingting Liu and Fang Yang*  \nCardiovascular Medicine Department, Yantaishan Hospital, Yantai, China  \nIntroduction: Acute myocardial infarction is a leading cause of global morbidity and mortality. Galectin-3, a β-galactoside-binding lectin, has been implicated as a key mediator in the pathophysiology following AMI. This review aims to synthesize the evidence on the multifaceted role of galectin-3, spanning from molecular mechanisms to clinical applications.  \nMethods: A comprehensive literature review was conducted to synthesize current evidence on the molecular functions, biomarker utility, and therapeutic targeting of galectin-3 in AMI. The analysis focused on studies investigating its signaling pathways, clinical correlations, and preclinical interventional models. Results: Our synthesis demonstrates that galectin-3 acts as a damageassociated molecular pattern that drives critical post-AMI pathologies. Mechanistically, it amplifies inflammation via NF-κB activation and macrophage polarization, promotes fibrosis through synergy with the TGF-β/Smad pathway and fibroblast activation, and regulates cardiomyocyte apoptosis and oxidative/endoplasmic reticulum stress. Clinically, its dynamic expression correlates with infarct size, adverse ventricular remodeling, and poor outcomes. As a biomarker, elevated circulating galectin-3 predicts major adverse cardiovascular events, heart failure, and mortality, improving risk stratification in multi-marker panels. Serial measurements indicate treatment response, with declining levels post-PCI or statin therapy associated with improved prognosis. Therapeutically, both genetic ablation and pharmacological inhibition of galectin-3 attenuate inflammation, fibrosis, and cardiac dysfunction in preclinical models.  \nDiscussion: Galectin-3 occupies a critical position at the intersection of AMI pathogenesis, diagnosis, and therapy. Targeting the galectin-3 pathway represents a promising therapeutic strategy to improve post-AMI outcomes, although its clinical translation requires further investigation. This review underscores the potential of integrating galectin-3 assessment and inhibition into future AMI management strategies.  \nKEYWORDS  \nacute myocardial infarction, apoptosis, cardiac remodeling, fibrosis, Galectin-3, inflammation, oxidative stress, therapeutic target  \nFrontiers in Molecular Biosciences 01 [frontiersin.org](frontiersin.org)  \n1 Introduction: epidemiology and pathophysiology of acute myocardial infarction  \nAcute myocardial infarction (AMI) remains a leading cause of global cardiovascular death, with 800000 annual cases and persistent 30-day mortality rates of 6%–8% despite reperfusion advances (Bhatt et al., 2022) . Critically, heart failure (HF) com","cbCaiptEsQGXuZeR","https://ap.wps.com/l/cbCaiptEsQGXuZeR","pdf",1780950,13,"English","# Introduction: epidemiology and pathophysiology of acute myocardial infarction\n## Methods: literature review scope on molecular functions, biomarker utility, and therapeutic targeting\n## Results: molecular mechanisms and clinical associations of Galectin-3\n## Discussion: clinical translation and future AMI management integration","[{\"question\":\"What role does galectin-3 play in AMI after injury?\",\"answer\":\"Galectin-3 functions as a damage-associated molecular pattern that drives key post-AMI pathologies, including inflammation, fibrosis, and regulation of apoptosis and cellular stress responses.\"},{\"question\":\"How is galectin-3 useful clinically in acute myocardial infarction?\",\"answer\":\"Elevated circulating galectin-3 correlates with infarct size, adverse ventricular remodeling, and poor outcomes, and serial measurements may reflect treatment response after PCI or statin therapy.\"},{\"question\":\"What evidence supports galectin-3 as a therapeutic target?\",\"answer\":\"Preclinical models show that genetic ablation or pharmacological inhibition of galectin-3 attenuates inflammation, fibrosis, and cardiac dysfunction, although clinical translation requires further investigation.\"}]","Galectin-3 in acute myocardial infarction: from molecular mechanisms to clinical translation | PDF",1790610325,33]