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Elevated Lp(a) increases risk of atherosclerotic cardiovascular disease, while its pathogenicity involves pro-atherogenic, pro-inflammatory, and pro-thrombotic mechanisms beyond cholesterol transport. This minireview synthesizes current knowledge on Lp(a) mechanisms, clinical implications, and the need for standardized measurement and emerging Lp(a)-targeted therapies.",{"@graph":14,"@context":73},[15,34,56],{"@type":16,"itemListElement":17},"BreadcrumbList",[18,23,27,31],{"item":19,"name":20,"@type":21,"position":22},"https://docshare.wps.com","Home","ListItem",1,{"item":24,"name":25,"@type":21,"position":26},"https://docshare.wps.com/document/","Document",2,{"item":28,"name":29,"@type":21,"position":30},"https://docshare.wps.com/document/healthcare/","Healthcare",3,{"item":32,"name":10,"@type":21,"position":33},"https://docshare.wps.com/document/lpa-in-the-horizon-of-diagnostics-and-therapy-review/465351/",4,{"url":32,"name":10,"@type":35,"image":36,"author":41,"headline":10,"publisher":44,"fileFormat":47,"inLanguage":8,"description":12,"dateModified":48,"datePublished":49,"encodingFormat":47,"isAccessibleForFree":50,"interactionStatistic":51},"DigitalDocument",{"url":37,"@type":38,"width":39,"height":40},"https://docshare.wps.com/thumbnails/lpa-in-the-horizon-of-diagnostics-and-therapy-review/465351.png","ImageObject",300,407,{"name":42,"@type":43},"Mia  ","Person",{"url":19,"name":45,"@type":46},"DocShare","Organization","application/pdf","2026-10-30","2026-09-30",true,{"@type":52,"interactionType":53,"userInteractionCount":55},"InteractionCounter",{"@type":54},"ViewAction",13,{"@type":57,"mainEntity":58},"FAQPage",[59,65,69],{"name":60,"@type":61,"acceptedAnswer":62},"Why is Lp(a) considered an independent cardiovascular risk factor?","Question",{"text":63,"@type":64},"Lp(a) levels are largely determined by genetics and are not adequately captured by conventional lipid profiling. Its concentration in the bloodstream is primarily driven by inherited biological factors.","Answer",{"name":66,"@type":61,"acceptedAnswer":67},"How does elevated Lp(a) contribute to cardiovascular events?",{"text":68,"@type":64},"Elevated Lp(a) is linked to a higher risk of atherosclerotic cardiovascular disease such as coronary artery disease, ischemic stroke, and calcific aortic valve stenosis. Mechanisms involve pro-atherogenic, pro-inflammatory, and pro-thrombotic effects, including interference with fibrinolysis.",{"name":70,"@type":61,"acceptedAnswer":71},"What makes measuring Lp(a) analytically challenging in clinical practice?",{"text":72,"@type":64},"Lp(a) has marked structural heterogeneity due to differences in apolipoprotein(a) isoforms. Variability in kringle IV type-2 repeats affects how isoforms interact with antibodies in immunoassays, creating discrepancies between laboratories and inconsistent reporting.","https://schema.org",{"og:url":32,"og:type":75,"og:title":10,"og:site_name":45,"og:description":12},"article",{"robots":77,"canonical":32},"index,follow",{"doc_id":79,"site_id":7},465351,1790812141,{"code":4,"msg":82,"data":83},"success",[84,88,92,96,101,106,110,115,120,123,127],{"id":22,"doc_module":4,"doc_module_name":25,"category_name":85,"show_sort_weight":86,"slug":87},"Story & Novel",90,"story-novel",{"id":26,"doc_module":4,"doc_module_name":25,"category_name":89,"show_sort_weight":90,"slug":91},"Literature",80,"literature",{"id":33,"doc_module":4,"doc_module_name":25,"category_name":93,"show_sort_weight":94,"slug":95},"Exam",70,"exam",{"id":97,"doc_module":4,"doc_module_name":25,"category_name":98,"show_sort_weight":99,"slug":100},5,"Comic",60,"comic",{"id":102,"doc_module":4,"doc_module_name":25,"category_name":103,"show_sort_weight":104,"slug":105},6,"Technology",50,"technology",{"id":107,"doc_module":4,"doc_module_name":25,"category_name":29,"show_sort_weight":108,"slug":109},7,40,"healthcare",{"id":111,"doc_module":4,"doc_module_name":25,"category_name":112,"show_sort_weight":113,"slug":114},8,"Research & Report",30,"research-report",{"id":116,"doc_module":4,"doc_module_name":25,"category_name":117,"show_sort_weight":118,"slug":119},9,"Religion & Spirituality",20,"religion-spirituality",{"id":118,"doc_module":4,"doc_module_name":25,"category_name":121,"show_sort_weight":118,"slug":122},"World Cup","world-cup",{"id":124,"doc_module":4,"doc_module_name":25,"category_name":125,"show_sort_weight":124,"slug":126},10,"Lifestyle","lifestyle",{"id":128,"doc_module":4,"doc_module_name":25,"category_name":129,"show_sort_weight":97,"slug":130},19,"General","general",{"code":4,"msg":82,"data":132},{"doc_id":79,"user_id":133,"nickname":42,"user_avatar":134,"doc_module":4,"category_id":107,"category_name":29,"doc_title":10,"doc_description":12,"doc_content":135,"file_id":136,"file_url":137,"file_type":138,"file_size":139,"view_count":55,"is_deleted":4,"is_public":22,"is_downloadable":22,"audit_status":22,"page_count":140,"language":141,"language_code":8,"site_id":7,"html_lang":8,"table_of_contents":142,"faqs":143,"seo_title":144,"seo_description":12,"update_tm":145,"read_time":146,"preview_page_count":4},687207024478,"https://ap-avatar.wpscdn.com/davatar_a8503ba1806abce46bf441b54a3ca4cd","Review  \nLp(a) in the Horizon of Diagnostics and Therapy  \nPietro Formisano 1, Elena Vianello 2,3, Elena Dozio 2,3, Lorenza Tacchini 2,3, Luigina Romani 4, Luigi Frati 5, Francesco Curcio 6,7, Marina Maria Bellet 8 and Massimiliano Marco Corsi-Romanelli 2,9, *  \nAcademic Editor: Kazufumi Nakamura  \nReceived: 20 November 2025  \nRevised: 23 December 2025  \nAccepted: 24 December 2025  \nPublished: 27 December 2025  \nCopyright: © 2025 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 Department of Translational Medicine, Federico II University of Naples, 80131 Naples, Italy  \n2 Department of Biomedical Sciences for Health, University of Milan, 20133 Milan, Italy  \n3 Experimental Laboratory for Research on Organ Damage Biomarkers, IRCCS Istituto Auxologico Italiano, 20149 Milan, Italy  \n4 Department of Experimental Medicine and Biochemical Sciences, University of Perugia, 06132 Perugia, Italy  \n5 Istituto di Ricovero e Cura a Carattere Scientifico (IRCCS) Neuromed, 86077 Pozzilli, Italy  \n6 Department of Medicine, University of Udine, 33100 Udine, Italy  \n7 Laboratory Medicine Department, Azienda Sanitaria Universitaria Friuli Centrale, 33100 Udine, Italy  \n8 Department of Medicine and Surgery, University of Perugia, P.le L. Severi 1, 06132 Perugia, Italy  \n9 Department of Experimental and Clinical Pathology, IRCCS Istituto Auxologico Italiano, 20149 Milan, Italy  \n* [Correspondence: mmcorsi@unimi.it](Correspondence: mmcorsi@unimi.it); Tel.: +39-3384895711  \nAbstract  \nLow-density lipoprotein cholesterol (LDL-C) has traditionally been the primary biomarker used to assess cardiovascular risk. However, a substantial proportion of cardiovascular events occur in individuals with LDL-C levels within the normal range, highlighting the need for additional risk markers. Lipoprotein(a) [Lp(a)] has emerged as an independent and genetically determined cardiovascular risk factor that is not adequately captured by conventional lipid profiling. Elevated Lp(a) levels are associated with an increased risk of atherosclerotic cardiovascular disease, including coronary artery disease, ischemic stroke, and calcific aortic valve stenosis, and appear to be particularly relevant in the context of premature cardiovascular events. The pathogenicity of Lp(a) is driven by distinct mechanisms that extend beyond cholesterol transport. These include pro-atherogenic, pro-inflammatory, and pro-thrombotic effects mediated largely by oxidized phospholipids carried by the particle and by the structural properties of apolipoprotein(a), which interfere with fibrinolysis. Despite its strong and stable genetic determination, Lp(a) remains underrecognized and inconsistently measured in clinical practice, partly due to historical limitations in assay standardization and reporting. This minireview summarizes current knowledge on the pathophysiological mechanisms underlying elevated Lp(a), discusses its clinical implications for cardiovascular risk assessment, and highlights the importance of standardized Lp(a) measurement in routine practice, particularly in light of emerging Lp(a)-targeted therapies.  \nKeywords: Lp(a); cardiovascular risk; therapy  \n1. Introduction  \nLipoprotein (a), usually abbreviated as Lp(a), is commonly referred to as “Lipoprotein little a.” Lp(a) bears a resemblance to low-density lipoprotein (LDL), except it contains an additional protein called “apolipoprotein A”(ApoA) [1,2] . Like LDL, which is a cholesterolrich lipoprotein, Lp(a) causes plaque formation in the arteries. The ApoA confers upon Lp(a) an additional characteristic, allowing it to display prothrombotic properties via an antifibrinolytic mechanism predominantly driven by ApoA. The combination of accelerated  \natherosclerotic progression and a prothrombotic effect results in a markedly increased risk of cardiovascular events [2,3] . Interestingly, Lp","cbCaihloITM0nFbF","https://ap.wps.com/l/cbCaihloITM0nFbF","pdf",245489,11,"English","# Introduction\n## Lp(a) as an independent cardiovascular risk factor\n# Analytical challenges and the need for standardization\n## Structural heterogeneity of Apo(a) and assay discrepancies","[{\"question\":\"Why is Lp(a) considered an independent cardiovascular risk factor?\",\"answer\":\"Lp(a) levels are largely determined by genetics and are not adequately captured by conventional lipid profiling. Its concentration in the bloodstream is primarily driven by inherited biological factors.\"},{\"question\":\"How does elevated Lp(a) contribute to cardiovascular events?\",\"answer\":\"Elevated Lp(a) is linked to a higher risk of atherosclerotic cardiovascular disease such as coronary artery disease, ischemic stroke, and calcific aortic valve stenosis. Mechanisms involve pro-atherogenic, pro-inflammatory, and pro-thrombotic effects, including interference with fibrinolysis.\"},{\"question\":\"What makes measuring Lp(a) analytically challenging in clinical practice?\",\"answer\":\"Lp(a) has marked structural heterogeneity due to differences in apolipoprotein(a) isoforms. Variability in kringle IV type-2 repeats affects how isoforms interact with antibodies in immunoassays, creating discrepancies between laboratories and inconsistent reporting.\"}]","Lp(a) in the Horizon of Diagnostics and Therapy - Review | PDF",1790769525,28]