Lipoprotein(a)-lowering therapies: a promising future.

Lipoprotein(a) possesses increased atherogenicity, contributing to residual cardiovascular risk.

脂蛋白(a) 具有增加的动脉粥样硬化性，是剩余心血管风险的贡献因素。

Elevated Lp(a) levels affect a substantial proportion of the population, rendering this a potentially high-impact therapeutic target, but currently available lipid-lowering agents and lifestyle interventions have minimal impact on lowering Lp(a), and lipoprotein apheresis is the sole effective-but impractical-method to significantly reduce Lp(a).

升高的脂蛋白(a) [Lp(a)]水平影响了相当一部分人群，使其成为一个潜在的高影响力治疗靶点，但目前可用的降脂药物和生活方式干预对降低Lp(a)几乎没有影响，而脂蛋白单采是唯一有效但不切实际的方法，可以显著降低Lp(a)。

Recent advances in Lp(a)-targeted therapies, notably nucleic acid-based approaches (e.g. antisense oligonucleotides and small interfering RNAs) and a small molecule inhibitor of Lp(a) synthesis, demonstrated substantial and often durable Lp(a)-lowering effects in Phase II trials.

最近在Lp(a)靶向治疗方面取得的进展，特别是基于核酸的方法（例如反义寡核苷酸和小干扰RNA）以及一种小分子Lp(a)合成抑制剂，在II期试验中显示出显著且往往持久的降低Lp(a)的效果。

Phase III trials of these agents are now underway to examine the impact of lowering Lp(a) levels on atherosclerotic cardiovascular disease outcomes, and their results may transform the landscape of cardiovascular risk reduction and management for patients with elevated Lp(a).

目前正在进行这些药物的III期试验，以检查降低Lp(a)水平对动脉粥样硬化心血管疾病结果的影响，其结果可能会改变高Lp(a)患者的降低心血管风险和管理的格局。

This review summarizes existing lipid-lowering therapies' limited effects on Lp(a), provides an update on the array of emerging therapeutics and their safety and efficacy, and discusses ongoing Phase III trials as well as other potential benefits of Lp(a)-lowering, such as slowing progression of calcific aortic valve stenosis.

本综述总结了现有降脂疗法对Lp(a)的有限影响，提供了新兴治疗药物及其安全性和有效性的最新信息，并讨论了正在进行的III期试验以及其他潜在的Lp(a)降低的好处，例如减缓钙化性主动脉瓣狭窄的进展。