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Lipoprotein(a) and its role in inflammation, atherosclerosis and malignancies.

作者信息

Orsó Evelyn, Schmitz Gerd

机构信息

Institute for Clinical Chemistry and Laboratory Medicine, University Hospital of Regensburg, Franz-Josef-Strauss-Allee 11, 93053, Regensburg, Germany.

出版信息

Clin Res Cardiol Suppl. 2017 Mar;12(Suppl 1):31-37. doi: 10.1007/s11789-017-0084-1.


DOI:10.1007/s11789-017-0084-1
PMID:28188431
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5352764/
Abstract

Lipoprotein (a) (Lp(a)) is a modified low-density lipoprotein (LDL) particle with an additional specific apolipoprotein (a), covalently attached to apolipoprotein B‑100 of LDL by a single thioester bond. Increased plasma Lp(a) level is a genetically determined, independent, causal risk factor for cardiovascular disease.The precise quantification of Lp(a) in plasma is still hampered by mass-sensitive assays, large particle variation, poor standardization and lack of assay comparability.The physiological functions of Lp(a) include wound healing, promoting tissue repair and vascular remodeling. Similarly to other lipoproteins, Lp(a) is also susceptible for oxidative modifications, leading to extensive formation of pro-inflammatory and pro-atherogenic oxidized phospholipids, oxysterols, oxidized lipid-protein adducts in Lp(a) particles, that perpetuate atherosclerotic lesion progression and intima-media thickening through induction of M1-macrophages, inflammation, autoimmunity and apoptosis. The oxidation-specific epitopes of modified lipoproteins are major targets of pre-immune, natural IgM antibodies, that may attenuate the pro-inflammatory and pro-atherogenic effects of Lp(a).Although the data are still insufficient, recent studies suggest a potential anti-neoplastic role of Lp(a).

摘要
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8a50/5352764/80824cec7c65/11789_2017_84_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8a50/5352764/80824cec7c65/11789_2017_84_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8a50/5352764/80824cec7c65/11789_2017_84_Fig1_HTML.jpg

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本文引用的文献

[1]
Increased Plasma IgE Accelerate Atherosclerosis in Secreted IgM Deficiency.

Circ Res. 2016-11-30

[2]
Lipoprotein (a) as a cause of cardiovascular disease: insights from epidemiology, genetics, and biology.

J Lipid Res. 2016-11

[3]
Prevalence of Elevated Lp(a) Mass Levels and Patient Thresholds in 532 359 Patients in the United States.

Arterioscler Thromb Vasc Biol. 2016-11

[4]
Lipoprotein(a) and vitamin C impair development of breast cancer tumors in Lp(a)+; Gulo-/- mice.

Int J Oncol. 2016-9

[5]
Oxidized Phospholipids on Lipoprotein(a) Elicit Arterial Wall Inflammation and an Inflammatory Monocyte Response in Humans.

Circulation. 2016-8-23

[6]
Lipoprotein (a) measurements for clinical application.

J Lipid Res. 2016-4

[7]
Mechanistic insights into Lp(a)-induced IL-8 expression: a role for oxidized phospholipid modification of apo(a).

J Lipid Res. 2015-12

[8]
Oxidized Phospholipids, Lipoprotein(a), and Progression of Calcific Aortic Valve Stenosis.

J Am Coll Cardiol. 2015-9-15

[9]
Alteration of serum lipid profile and its prognostic value in head and neck squamous cell carcinoma.

J Oral Pathol Med. 2016-3

[10]
Lipoprotein(a) hyperlipidemia as cardiovascular risk factor: pathophysiological aspects.

Clin Res Cardiol Suppl. 2015-4

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