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Lipoprotein(a) in Cardiovascular Diseases

Lipoprotein(a) (Lp(a)) is an LDL-like molecule consisting of an apolipoprotein B-100 (apo(B-100)) particle attached by a disulphide bridge to apo(a). Many observations have pointed out that Lp(a) levels may be a risk factor for cardiovascular diseases. Lp(a) inhibits the activation of transforming g...

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Autores principales: Malaguarnera, Michele, Vacante, Marco, Russo, Cristina, Malaguarnera, Giulia, Antic, Tijana, Malaguarnera, Lucia, Bella, Rita, Pennisi, Giovanni, Galvano, Fabio, Frigiola, Alessandro
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi Publishing Corporation 2013
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3591100/
https://www.ncbi.nlm.nih.gov/pubmed/23484137
http://dx.doi.org/10.1155/2013/650989
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author Malaguarnera, Michele
Vacante, Marco
Russo, Cristina
Malaguarnera, Giulia
Antic, Tijana
Malaguarnera, Lucia
Bella, Rita
Pennisi, Giovanni
Galvano, Fabio
Frigiola, Alessandro
author_facet Malaguarnera, Michele
Vacante, Marco
Russo, Cristina
Malaguarnera, Giulia
Antic, Tijana
Malaguarnera, Lucia
Bella, Rita
Pennisi, Giovanni
Galvano, Fabio
Frigiola, Alessandro
author_sort Malaguarnera, Michele
collection PubMed
description Lipoprotein(a) (Lp(a)) is an LDL-like molecule consisting of an apolipoprotein B-100 (apo(B-100)) particle attached by a disulphide bridge to apo(a). Many observations have pointed out that Lp(a) levels may be a risk factor for cardiovascular diseases. Lp(a) inhibits the activation of transforming growth factor (TGF) and contributes to the growth of arterial atherosclerotic lesions by promoting the proliferation of vascular smooth muscle cells and the migration of smooth muscle cells to endothelial cells. Moreover Lp(a) inhibits plasminogen binding to the surfaces of endothelial cells and decreases the activity of fibrin-dependent tissue-type plasminogen activator. Lp(a) may act as a proinflammatory mediator that augments the lesion formation in atherosclerotic plaques. Elevated serum Lp(a) is an independent predictor of coronary artery disease and myocardial infarction. Furthermore, Lp(a) levels should be a marker of restenosis after percutaneous transluminal coronary angioplasty, saphenous vein bypass graft atherosclerosis, and accelerated coronary atherosclerosis of cardiac transplantation. Finally, the possibility that Lp(a) may be a risk factor for ischemic stroke has been assessed in several studies. Recent findings suggest that Lp(a)-lowering therapy might be beneficial in patients with high Lp(a) levels. A future therapeutic approach could include apheresis in high-risk patients in order to reduce major coronary events.
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spelling pubmed-35911002013-03-12 Lipoprotein(a) in Cardiovascular Diseases Malaguarnera, Michele Vacante, Marco Russo, Cristina Malaguarnera, Giulia Antic, Tijana Malaguarnera, Lucia Bella, Rita Pennisi, Giovanni Galvano, Fabio Frigiola, Alessandro Biomed Res Int Review Article Lipoprotein(a) (Lp(a)) is an LDL-like molecule consisting of an apolipoprotein B-100 (apo(B-100)) particle attached by a disulphide bridge to apo(a). Many observations have pointed out that Lp(a) levels may be a risk factor for cardiovascular diseases. Lp(a) inhibits the activation of transforming growth factor (TGF) and contributes to the growth of arterial atherosclerotic lesions by promoting the proliferation of vascular smooth muscle cells and the migration of smooth muscle cells to endothelial cells. Moreover Lp(a) inhibits plasminogen binding to the surfaces of endothelial cells and decreases the activity of fibrin-dependent tissue-type plasminogen activator. Lp(a) may act as a proinflammatory mediator that augments the lesion formation in atherosclerotic plaques. Elevated serum Lp(a) is an independent predictor of coronary artery disease and myocardial infarction. Furthermore, Lp(a) levels should be a marker of restenosis after percutaneous transluminal coronary angioplasty, saphenous vein bypass graft atherosclerosis, and accelerated coronary atherosclerosis of cardiac transplantation. Finally, the possibility that Lp(a) may be a risk factor for ischemic stroke has been assessed in several studies. Recent findings suggest that Lp(a)-lowering therapy might be beneficial in patients with high Lp(a) levels. A future therapeutic approach could include apheresis in high-risk patients in order to reduce major coronary events. Hindawi Publishing Corporation 2013 2012-12-30 /pmc/articles/PMC3591100/ /pubmed/23484137 http://dx.doi.org/10.1155/2013/650989 Text en Copyright © 2013 Michele Malaguarnera et al. https://creativecommons.org/licenses/by/3.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Review Article
Malaguarnera, Michele
Vacante, Marco
Russo, Cristina
Malaguarnera, Giulia
Antic, Tijana
Malaguarnera, Lucia
Bella, Rita
Pennisi, Giovanni
Galvano, Fabio
Frigiola, Alessandro
Lipoprotein(a) in Cardiovascular Diseases
title Lipoprotein(a) in Cardiovascular Diseases
title_full Lipoprotein(a) in Cardiovascular Diseases
title_fullStr Lipoprotein(a) in Cardiovascular Diseases
title_full_unstemmed Lipoprotein(a) in Cardiovascular Diseases
title_short Lipoprotein(a) in Cardiovascular Diseases
title_sort lipoprotein(a) in cardiovascular diseases
topic Review Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3591100/
https://www.ncbi.nlm.nih.gov/pubmed/23484137
http://dx.doi.org/10.1155/2013/650989
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