ReviewCurrent atherosclerosis reports2013
Update on lipoprotein(a) as a cardiovascular risk factor and mediator.
Review in Current atherosclerosis reports, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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
15 citing papers in PubMed, 36 citations in OpenAlex.
- Lipoprotein(a) accelerated the progression of atherosclerosis in patients with end-stage renal disease.BMC nephrology · 2018Trial
- Comparison of lipid and lipid-associated cardiovascular risk marker changes after treatment with tocilizumab or adalimumab in patients with rheumatoid arthritis.Annals of the rheumatic diseases · 2016Trial
- Lipoprotein(a) in Coronary Artery Disease and Aortic Stenosis: Pathophysiology, Clinical Impact, Interventional Implications and Emerging Targeted Therapies.Journal of clinical medicine · 2026Review
- Elevated lipoprotein(a) and cardiovascular outcomes in prediabetes and diabetes: a systematic review and meta-analysis.Cardiovascular diagnosis and therapy · 2025Article
- Lipoprotein(a) and Its Role in Peripheral Arterial Disease: A Narrative Review.Vascular health and risk management · 2025Review
- Novel Therapeutic Approaches for the Management of Elevated Lipoprotein(a): From Traditional Agents to Future Treatment Options.Life (Basel, Switzerland) · 2024Review
- Modern Approaches to Lower Lipoprotein(a) Concentrations and Consequences for Cardiovascular Diseases.Biomedicines · 2021Review
- Current Evidence and Future Directions of PCSK9 Inhibition.US cardiology · 2021Review
- Prevalence and status of Lipoprotein (a) among Lebanese school children.Scientific reports · 2020Article
- Lipoprotein(a): An Enigmatic Sheep in the Lipoprotein Herd.JACC. Basic to translational science · 2020Article
- PCSK9: From Basic Science Discoveries to Clinical Trials.Circulation research · 2018Review
- Lipoprotein(a): A Lipoprotein Whose Time Has Come.Current treatment options in cardiovascular medicine · 2017Review
- Lipoprotein (a) level, apolipoprotein (a) size, and risk of unexplained ischemic stroke in young and middle-aged adults.Atherosclerosis · 2016Article
- Distinct metabolism of apolipoproteins (a) and B-100 within plasma lipoprotein(a).Metabolism: clinical and experimental · 2016Article
- Lipoprotein(a) catabolism is regulated by proprotein convertase subtilisin/kexin type 9 through the low density lipoprotein receptor.The Journal of biological chemistry · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Recent genetic studies have put the spotlight back onto lipoprotein(a) [Lp(a)] as a causal risk factor for coronary heart disease. However, there remain significant gaps in our knowledge with respect to how the Lp(a) particle is assembled, the route of its catabolism, and the mechanism(s) of Lp(a) pathogenicity. It has long been speculated that the effects of Lp(a) in the vasculature can be attributed to both its low-density lipoprotein moiety and the unique apolipoprotein(a) component, which is strikingly similar to the kringle-containing fibrinolytic zymogen plasminogen. However, the ability of Lp(a) to modulate either purely thrombotic or purely atherothrombotic processes in vivo remains unclear. The presence of oxidized phospholipid on Lp(a) may underlie many of the proatherosclerotic effects of Lp(a) that have been identified both in cell models and in animal models, and provides a possible avenue for identifying therapeutics aimed at mitigating the effects of Lp(a) in the vasculature. However, the beneficial effects of targeted Lp(a) therapeutics, designed to either lower Lp(a) concentrations or interfere with its effects, on cardiovascular outcomes remains to be determined.
Indexed as
Identifiers
What 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.