Enigmatic role of lipoprotein(a) in cardiovascular disease.
Open accessAbstract
Lipoprotein (a), [Lp(a)] has many properties in common with low-density lipoprotein, (LDL) but contains a unique protein apolipoprotein(a), linked to apolipoprotein B-100 by a single disulfide bond. There is a substantial size heterogeneity of apo(a), and generally smaller apo(a) sizes tend to correspond to higher plasma Lp(a) levels, but this relation is far from linear, underscoring the importance to assess allele-specific apo(a) levels. The presence of apo(a), a highly charged, carbohydrate-rich, hydrophilic protein may obscure key features of the LDL moiety and offer opportunities for binding to vessel wall elements. Recently, interest in Lp(a) has increased because studies over the past decade have confirmed and more robustly demonstrated a risk factor role of Lp(a) for cardiovascular disease. In particular, levels of Lp(a) carried in particles with smaller size apo(a) isoforms are associated with coronary artery disease (CAD). Other studies suggest that proinflammatory conditions may modulate risk factor properties of Lp(a). Further, Lp(a) may act as a preferential acceptor for proinflammatory oxidized phospholipids transferred from tissues or from other lipoproteins. However, at present only a limited number of agents (e.g., nicotinic acid and estrogen) has proven efficacy in lowering Lp(a) levels. Although Lp(a) has not been definitely established as a cardiovascular risk factor and no guidelines presently recommend intervention, Lp(a)-lowering therapy might offer benefits in subgroups of patients with high Lp(a) levels.
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Studies over the past decade have confirmed and more robustly demonstrated a risk factor role of Lp(a) for cardiovascular disease.
“Recently, interest in Lp(a) has increased because studies over the past decade have confirmed and more robustly demonstrated a risk factor role of Lp(a) for cardiovascular disease (43-46).”
From Evaluation and Treatment of Hypertriglyceridemia: An Endocrine Society Clinical Practice Guideline (2012) · cites this paper as [46]
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Self-citationCarboxyl‐terminal truncation of apolipoproteinB‐100 inhibits lipoprotein(a) particle formation
Gabel, B. R., Yao, Z., McLeod, R. S., et al. (1994) · FEBS Letters · doi:10.1016/0014-5793(94)00737-3 · Cited by 30 · see citing works
Postmenopausal Hormone Replacement Therapy with Tibolone Decreases Serum Lipoprotein(a)
Hænggi, W., Riesen, W., & Birkhaeuser, M. H. (1993) · Clinical Chemistry and Laboratory Medicine (CCLM) · doi:10.1515/cclm.1993.31.10.645 · Cited by 30 · see citing works
Zeljković, A., Bogavac‐Stanojević, N., Jelić‐Ivanović, Z., Spasojević‐Kalimanovska, V., Vekić, J., & Spasić, S. (2008) · Archives of Medical Research · doi:10.1016/j.arcmed.2008.10.010 · Cited by 19 · see citing works
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Evaluation and Treatment of Hypertriglyceridemia: An Endocrine Society Clinical Practice Guideline
Berglund, L., Brunzell, J. D., Goldberg, A. C., Goldberg, I. J., Sacks, F., Murad, M. H., & Stalenhoef, A. F. H. (2012) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jc.2011-3213 · Cited by 887 · see citing works
Self-citation
- Authors
- Anuurad, E., Enkhmaa, B., & Berglund, L.
- Affiliations
- University of California, Davis (US)
- VA Northern California Health Care System (US)
- Venue
- Clinical and Translational Science
- Publisher
- Wiley
- Published
- 2010-12
- Volume
- 3
- Issue
- 6
- Pages
- 327-332
- ISSN
- 1752-8054 (ISSN-L)
- 1752-8062
- PMC
- PMC3075492
- OpenAlex
- W1984201082
- Cited by
- 14
- References
- 97
- Citations by year
- 2022: 2 · 2020: 1 · 2015: 1 · 2013: 6 · 2012: 2
- FWCI
- 3.38
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Clinical and Translational Science (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- University of California, Davis
- National Heart, Lung, and Blood Institute (HL62705, HL65938, R01HL062705, R01HL065938)
- National Center for Research Resources (RR-024146, K12 RR024144, UL1RR024146, KL2RR024144)
- Topics
- Health Sciences › Medicine › Surgery › Lipoproteins and Cardiovascular Health
- Health Sciences › Medicine › Surgery › Cholesterol and Lipid Metabolism
- Life Sciences › Immunology and Microbiology › Immunology › Atherosclerosis and Cardiovascular Diseases
- Keywords
- lipoprotein(a), apolipoprotein(a), cardiovascular disease, coronary artery disease, apolipoprotein(a) isoforms, oxidized phospholipids, inflammation, low-density lipoprotein, cardiovascular risk factors, Lp(a)-lowering therapy, nicotinic acid, estrogen
- MeSH terms
- Alleles, Apolipoproteins A, Cardiovascular Diseases, Humans, Inflammation, Risk Factors, Lipoprotein(a), Atherosclerosis
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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