ReviewCurrent atherosclerosis reports2026
Old and New Lines of Therapy Targeting Lipoprotein(a).
Review in Current atherosclerosis reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purpose of reviewElevated lipoprotein(a) (Lp[a]) is a prevalent, lifelong, and genetically determined causal cardiovascular risk factor, associated with a wide spectrum of cardiovascular disease, including atherosclerotic coronary artery disease, aortic stenosis, ischemic stroke, and peripheral vascular disease. This review aims to: examine the evolving therapeutic landscape for Lp(a), concisely summarize results from preclinical work and ongoing clinical trials of novel pharmacologic and gene-based therapies, and contextualize their potential role in cardiovascular disease prevention. RECENT
findingsRandomized clinical trials are now underway for several promising therapeutics targeting LPA gene translation, including antisense oligonucleotides (pelacarsen) and small interfering RNAs (olpasiran, lepodisiran, zerlasiran), with the earliest of these expected to read out in 2026. An oral small-molecule inhibitor (muvalaplin) has also demonstrated substantial Lp(a) lowering by disrupting apo(a)-apoB assembly. In parallel, gene-editing approaches using CRISPR/Cas9 have shown durable suppression of LPA expression in preclinical models, although these therapies remain at an early, proof-of-concept stage. Large, randomized phase 3 clinical trials are ongoing to determine whether significant reductions in Lp(a) will result in a meaningful reduction in downstream clinical events. Lp(a) is an important cardiovascular risk factor for which no approved targeted therapies currently exist. Universal one-time Lp(a) screening is increasingly recommended, underscoring a growing gap between risk identification and mitigation. A robust pipeline of Lp(a)-lowering therapies - spanning injectable gene-silencing therapeutics, oral small molecules, and next-generation gene-editing technologies - has the potential to fundamentally alter our current risk prevention paradigm. The results of these ongoing clinical trials will be crucial in determining whether targeted Lp(a) reduction can meaningfully reduce residual cardiovascular risk and establish Lp(a) as a modifiable risk factor in both primary and secondary prevention.
Indexed as
Identifiers
42234287What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.