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Purpose <p>Lipoprotein(a) [Lp(a)] is increasingly recognized as a genetically determined, independent risk factor for atherosclerotic&#xa0;cardiovascular disease (ASCVD). This review examines the structure, pathophysiology, and epidemiology of Lp(a), with a focus on its&#xa0;contribution to ASCVD and related conditions such as aortic valve stenosis and peripheral artery disease. The main research&#xa0;question addresses how Lp(a) influences cardiovascular risk and how emerging therapies may modify this risk.</p> Methods <p>This review synthesizes published evidence describing the biological characteristics of Lp(a), its mechanistic roles in disease, and its&#xa0;epidemiologic associations with cardiovascular outcomes. It also evaluates current and investigational therapeutic approaches by&#xa0;examining clinical trial data for agents targeting Lp(a).</p> Results <p>Lp(a) contributes to residual cardiovascular risk through proatherogenic, proinflammatory, and prothrombotic mechanisms. Current&#xa0;evidence highlights its involvement in ASCVD, aortic valve stenosis, and peripheral artery disease. Clinical studies of antisense&#xa0;oligonucleotides, small interfering RNAs, oral small molecules, and CRISPR-based gene editing, including pelacarsen, olpasiran,&#xa0;zerlasiran, lepodisiran, muvalaplin, and obicetrapib, demonstrate promising efficacy and safety. These agents show potential to&#xa0;significantly reduce Lp(a) levels and influence future cardiovascular prevention strategies.</p> Conclusion <p>As novel therapies advance and clinical guidelines evolve, Lp(a) is emerging as a central determinant in personalized cardiovascular&#xa0;care. The increasing emphasis on Lp(a) testing underscores its importance in risk stratification and future therapeutic decisionmaking.</p>

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Lipoprotein(a) in Cardiovascular Diseases and Emerging Therapeutic Strategies

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年11月20日

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  • Rami A. Al-Horani,
  • Alexandra C. Selico-Dunn,
  • Emily Lauren Schenk Smith

摘要

Purpose

Lipoprotein(a) [Lp(a)] is increasingly recognized as a genetically determined, independent risk factor for atherosclerotic cardiovascular disease (ASCVD). This review examines the structure, pathophysiology, and epidemiology of Lp(a), with a focus on its contribution to ASCVD and related conditions such as aortic valve stenosis and peripheral artery disease. The main research question addresses how Lp(a) influences cardiovascular risk and how emerging therapies may modify this risk.

Methods

This review synthesizes published evidence describing the biological characteristics of Lp(a), its mechanistic roles in disease, and its epidemiologic associations with cardiovascular outcomes. It also evaluates current and investigational therapeutic approaches by examining clinical trial data for agents targeting Lp(a).

Results

Lp(a) contributes to residual cardiovascular risk through proatherogenic, proinflammatory, and prothrombotic mechanisms. Current evidence highlights its involvement in ASCVD, aortic valve stenosis, and peripheral artery disease. Clinical studies of antisense oligonucleotides, small interfering RNAs, oral small molecules, and CRISPR-based gene editing, including pelacarsen, olpasiran, zerlasiran, lepodisiran, muvalaplin, and obicetrapib, demonstrate promising efficacy and safety. These agents show potential to significantly reduce Lp(a) levels and influence future cardiovascular prevention strategies.

Conclusion

As novel therapies advance and clinical guidelines evolve, Lp(a) is emerging as a central determinant in personalized cardiovascular care. The increasing emphasis on Lp(a) testing underscores its importance in risk stratification and future therapeutic decisionmaking.