The DOI matches its Crossref record; 204 of the 204 references it cites were found in a registry or an index.
Lipoprotein(a): resurrected by genetics
Open accessAbstract
Plasma lipoprotein(a) [L p(a)] is a quantitative genetic trait with a very broad and skewed distribution, which is largely controlled by genetic variants at the LPA locus on chromosome 6q27. Based on genetic evidence provided by studies conducted over the last two decades, L p(a) is currently considered to be the strongest genetic risk factor for coronary heart disease (CHD). The copy number variation of kringle IV in the LPA gene has been strongly associated with both L p(a) levels in plasma and risk of CHD, thereby fulfilling the main criterion for causality in a M endelian randomization approach. Alleles with a low kringle IV copy number that together have a population frequency of 25–35% are associated with a doubling of the relative risk for outcomes, which is exceptional in the field of complex genetic phenotypes. The recently identified binding of oxidized phospholipids to L p(a) is considered as one of the possible mechanisms that may explain the pathogenicity of L p(a). Drugs that have been shown to lower L p(a) have pleiotropic effects on other CHD risk factors, and an improvement of cardiovascular endpoints is up to now lacking. However, it has been established in a proof of principle study that lowering of very high L p(a) by apheresis in high‐risk patients with already maximally reduced low‐density lipoprotein cholesterol levels can dramatically reduce major coronary events.
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“[Statement]Hyper-Lp(a)-lipoproteinemia is a risk factor for ASCVD. (Evidence level: E-1a)”
From Japan Atherosclerosis Society (JAS) guidelines for prevention of atherosclerotic cardiovascular diseases 2017 (2018) · cites this paper as [221]
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“When the size of apolipoprotein (a) [apo(a)] is small, the concentration of Lp(a) is high, and there is a high risk of CVD.”
From Japan Atherosclerosis Society (JAS) guidelines for prevention of atherosclerotic cardiovascular diseases 2017 (2018) · cites this paper as [221]
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“Lp(a) is an independent risk factor for CAD and stroke.”
From Japan Atherosclerosis Society (JAS) guidelines for prevention of atherosclerotic cardiovascular diseases 2017 (2018) · cites this paper as [221]
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- 10.1210/jc.81.7.2633 · DOI
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Metadata
- Authors
- Kronenberg, F., & Utermann, G.
- Affiliations
- Innsbruck Medical University (AT)
- Corresponding author
- Utermann, G.
- ORCID
- Kronenberg, F.
- Venue
- Journal of Internal Medicine
- Publisher
- Wiley
- Published
- 2012-11-12
- Volume
- 273
- Issue
- 1
- Pages
- 6-30
- ISSN
- 0954-6820 (ISSN-L)
- 1365-2796
- OpenAlex
- W1988877980
- Cited by
- 521
- References
- 203
- Citations by year
- 2026: 40 · 2025: 38 · 2024: 39 · 2023: 41 · 2022: 45 · 2021: 42 · 2020: 36 · 2019: 48 · 2018: 35 · 2017: 36 · 2016: 42 · 2015: 38 · 2014: 20 · 2013: 17 · 2012: 2
- FWCI
- 4.75
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Internal Medicine (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Austrian Science Fund
- Oesterreichische Nationalbank
- Standortagentur Tirol
- Topics
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Lipoproteins and Cardiovascular Health
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetic Associations and Epidemiology
- Life Sciences › Immunology and Microbiology › Immunology › Atherosclerosis and Cardiovascular Diseases
- Keywords
- lipoprotein(a), LPA gene, coronary heart disease risk, genetic risk factors, Mendelian randomization, apheresis, cardiovascular risk reduction
- MeSH terms
- Alleles, Coronary Artery Disease, DNA, Gene Frequency, Humans, Polymorphism, Genetic, Lipoprotein(a), Genetic Predisposition to Disease, Mendelian Randomization Analysis
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