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A clinician-focused review consolidates Lp(a)'s path from biomarker discovery to emerging targeted therapy (Am J Cardiol 2025)

Original title: Lipoprotein(a) - From Biomarker to Therapy: A Review for the Clinician

Am J Cardiol · · 5

Jha M, McCarthy IR, Gelfand EV

This review consolidates current knowledge on Lp(a), from its biological role to its clinical implications, for practising clinicians. It frames Lp(a) as a critical biomarker for identifying elevated risk of atherosclerotic cardiovascular disease and calcific aortic valve stenosis independent of traditional risk factors, describing how its apolipoprotein(a) component, genetically determined and shared no meaningful modulation by lifestyle, drives vascular inflammation, atherogenesis, calcification and thrombosis. The authors survey emerging antisense oligonucleotide and small interfering RNA therapies now shown to lower Lp(a), with ongoing trials assessing whether this reduces cardiovascular disease risk, and note that screening and management guidelines continue to evolve as these targeted therapies advance, potentially transforming both prevention and treatment of Lp(a)-associated cardiovascular disease.

Read the paper (DOI)PubMed

Original abstract

Cardiovascular disease (CVD) remains the predominant cause of morbidity and mortality globally. Amid rising CVD rates, Lipoprotein(a) [Lp(a)] has been recognized as a critical biomarker identifying individuals at an increased risk of atherosclerotic cardiovascular disease (ASCVD) and calcific aortic valve stenosis (AS), independent of traditional risk factors. Lp(a) is a lipoprotein variant similar to LDL but includes apolipoprotein(a), which influences its pathogenic potential. Elevated Lp(a) levels are genetically determined and have been implicated in promoting vascular inflammation, atherogenesis, enhanced calcification, and thrombosis. Emerging antisense oligonucleotide (ASO)- and small interfering ribonucleic acids (siRNAs)- based therapies have been shown to lower Lp(a) concentrations, with ongoing trials underway to determine whether they reduce the risk of CVD. While guidelines on screening and management continue to evolve, the advent of specific Lp(a)-lowering therapies may transform CVD prevention and treatment. This review aims to consolidate the current knowledge on Lp(a) from its biological functions to its implications for clinical practice, focusing on its role as a biomarker and potential therapeutic target.

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Summary written by lp-a.org from the published abstract; figures as published. Page updated 17 August 2026. Methods.