ReviewCirculation research2019
Potential Causality and Emerging Medical Therapies for Lipoprotein(a) and Its Associated Oxidized Phospholipids in Calcific Aortic Valve Stenosis.
Review in Circulation research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 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
38 citing papers in PubMed, 83 citations in OpenAlex.
- Potent reduction of plasma lipoprotein (a) with an antisense oligonucleotide in human subjects does not affect ex vivo fibrinolysis.Journal of lipid research · 2019Trial
- The Association Between Lipoprotein(a) and Atherosclerotic Cardiovascular Disease Severity.Reviews in cardiovascular medicine · 2026Article
- Orphan Nuclear Receptor NR4A1 Promotes Proliferation and Osteogenic Differentiation of Valvular Interstitial Cells through Activation of CCND2.International journal of biological sciences · 2026Article
- Lipoprotein(a) in clinical practice: Risk stratification and therapeutic strategies.European journal of clinical investigation · 2026Review
- Mechanistic Insights into Bioprosthetic Heart Valve Calcification and Anti-Calcification Strategies.Reviews in cardiovascular medicine · 2025Review
- Atherosclerosis, calcific aortic valve disease and mitral annular calcification: same or different?International journal of cardiology · 2025Review
- Association Between Lipoprotein(a) and Dilatation of Different Aortic Segments in Hypertensive Patients.Echocardiography (Mount Kisco, N.Y.) · 2025Article
- LDL atherogenicity determined by size, density, oxidation, apolipoprotein(a), and electronegativity: an updated review.Frontiers in cardiovascular medicine · 2025Review
- Role of Lipoprotein (A) in aortic valve stenosis: Novel disease mechanisms and emerging pharmacotherapeutic approaches.International journal of cardiology. Heart & vasculature · 2024Review
- The functions of apolipoproteins and lipoproteins in health and disease.Molecular biomedicine · 2024Review
- Lipoprotein(a) Levels in Severe Aortic Stenosis Referred for Transcatheter Aortic Valve Implantation Compared to Controls.JACC. Advances · 2024Article
- FOXO1 regulates RUNX2 ubiquitination through SMURF2 in calcific aortic valve disease.Redox biology · 2024Article
- Associations between lipoprotein(a), oxidized phospholipids, and extracoronary vascular disease.Journal of lipid research · 2024Article
- TRPM4 mRNA stabilization by METTL3-mediated m6A modification promotes calcific aortic valve inflammation.Heliyon · 2024Article
- Lipoprotein(a)'s Role in Atherosclerosis and Aortic Stenosis: A Contemporary Literature Review.Cureus · 2024Review
- Treatment of Lp(a): Is It the Future or Are We Ready Today?Current atherosclerosis reports · 2023Review
- Lipoprotein(a): Just an Innocent Bystander in Arterial Hypertension?International journal of molecular sciences · 2023Review
- Atherosclerosis Calcification: Focus on Lipoproteins.Metabolites · 2023Review
- Pathophysiology, emerging techniques for the assessment and novel treatment of aortic stenosis.Open heart · 2023Review
- Lipoprotein(a) in atherosclerotic cardiovascular disease and aortic stenosis: a European Atherosclerosis Society consensus statement.European heart journal · 2022Article
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
The prevalence of calcific aortic valve disease is increasing with aging of the population. Current treatment options for advanced or symptomatic aortic stenosis are limited to traditional surgical or percutaneous aortic valve replacement. Medical therapies that impact the progression of calcific aortic valve disease do not currently exist. New pathophysiological insights suggest that the processes leading to calcific aortic valve disease are metabolically active for many years before and during the clinical expression of disease. The identification of genetic and potentially causal mediators of calcific aortic valve disease allows opportunities for therapies that may slow progression to the point where aortic valve replacement can be avoided. Recent studies suggest that approximately one-third of aortic stenosis cases are associated with highly elevated lipoprotein(a) [Lp(a)] and pathways related to the metabolism of procalcifying oxidized phospholipids. Oxidized phospholipids can be carried by Lp(a) into valve leaflets but can also be formed in situ from cell membranes, lipoproteins, and apoptotic cells. This review will summarize the clinical data implicating the potential causality of Lp(a)/oxidized phospholipids, describe emerging therapeutic agents, and propose clinical trial designs to test the hypothesis that lowering Lp(a) will reduce progression aortic stenosis and the need for aortic valve replacement.
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What OpenQuestion 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 OpenQuestion graph.