Abstract
Epidemiological and clinical studies have demonstrated the inverse association between HDL cholesterol levels (HDL-C) and the risk of coronary heart disease (CHD). This correlation is believed to relate to the ability of HDL to promote reverse cholesterol transport. Remodeling of HDL due to chemical/physical modifications can dramatically affect its functions, leading to dysfunctional HDL that could promote atherogenesis. HDL modification can be achieved by different means: (i) non-enzymatic modifications, owing to the presence of free metal ions in the atherosclerotic plaques; (ii) cell-associated enzymes, which can degrade the apoproteins without significant changes in the lipid moiety, or can alternatively induce apoprotein cross-linking and lipid oxidation; (iii) association with acute phase proteins, whose circulating levels are significantly increased during inflammation which may modify HDL structure and functions; and (iv) metabolic modifications, such as glycation that occurs under hyperglycaemic conditions. Available data suggest that HDL can easily be modified losing their anti-atherogenic activities. These observation results mainly from in vitro studies, while few in vivo data, are available. Furthermore the in vivo mechanisms involved in HDL modification are ill understood. A better knowledge of these pathways may provide possible therapeutic target aimed at reducing HDL modification.
| Original language | English |
|---|---|
| Pages (from-to) | 371-386 |
| Number of pages | 16 |
| Journal | Nutrition, Metabolism and Cardiovascular Diseases |
| Volume | 16 |
| Issue number | 5 |
| DOIs | |
| Publication status | Published - Jul 2006 |
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Keywords
- Glycation
- Modified HDL
- Myeloperoxidase
- Paraoxonase
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine
- Medicine (miscellaneous)
- Food Science
- Endocrinology, Diabetes and Metabolism
Cite this
Modified HDL : Biological and physiopathological consequences. / Norata, Giuseppe Danilo; Pirillo, Angela; Catapano, Alberico Luigi.
In: Nutrition, Metabolism and Cardiovascular Diseases, Vol. 16, No. 5, 07.2006, p. 371-386.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Modified HDL
T2 - Biological and physiopathological consequences
AU - Norata, Giuseppe Danilo
AU - Pirillo, Angela
AU - Catapano, Alberico Luigi
PY - 2006/7
Y1 - 2006/7
N2 - Epidemiological and clinical studies have demonstrated the inverse association between HDL cholesterol levels (HDL-C) and the risk of coronary heart disease (CHD). This correlation is believed to relate to the ability of HDL to promote reverse cholesterol transport. Remodeling of HDL due to chemical/physical modifications can dramatically affect its functions, leading to dysfunctional HDL that could promote atherogenesis. HDL modification can be achieved by different means: (i) non-enzymatic modifications, owing to the presence of free metal ions in the atherosclerotic plaques; (ii) cell-associated enzymes, which can degrade the apoproteins without significant changes in the lipid moiety, or can alternatively induce apoprotein cross-linking and lipid oxidation; (iii) association with acute phase proteins, whose circulating levels are significantly increased during inflammation which may modify HDL structure and functions; and (iv) metabolic modifications, such as glycation that occurs under hyperglycaemic conditions. Available data suggest that HDL can easily be modified losing their anti-atherogenic activities. These observation results mainly from in vitro studies, while few in vivo data, are available. Furthermore the in vivo mechanisms involved in HDL modification are ill understood. A better knowledge of these pathways may provide possible therapeutic target aimed at reducing HDL modification.
AB - Epidemiological and clinical studies have demonstrated the inverse association between HDL cholesterol levels (HDL-C) and the risk of coronary heart disease (CHD). This correlation is believed to relate to the ability of HDL to promote reverse cholesterol transport. Remodeling of HDL due to chemical/physical modifications can dramatically affect its functions, leading to dysfunctional HDL that could promote atherogenesis. HDL modification can be achieved by different means: (i) non-enzymatic modifications, owing to the presence of free metal ions in the atherosclerotic plaques; (ii) cell-associated enzymes, which can degrade the apoproteins without significant changes in the lipid moiety, or can alternatively induce apoprotein cross-linking and lipid oxidation; (iii) association with acute phase proteins, whose circulating levels are significantly increased during inflammation which may modify HDL structure and functions; and (iv) metabolic modifications, such as glycation that occurs under hyperglycaemic conditions. Available data suggest that HDL can easily be modified losing their anti-atherogenic activities. These observation results mainly from in vitro studies, while few in vivo data, are available. Furthermore the in vivo mechanisms involved in HDL modification are ill understood. A better knowledge of these pathways may provide possible therapeutic target aimed at reducing HDL modification.
KW - Glycation
KW - Modified HDL
KW - Myeloperoxidase
KW - Paraoxonase
UR - http://www.scopus.com/inward/record.url?scp=33745610718&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=33745610718&partnerID=8YFLogxK
U2 - 10.1016/j.numecd.2006.01.012
DO - 10.1016/j.numecd.2006.01.012
M3 - Article
C2 - 16829346
AN - SCOPUS:33745610718
VL - 16
SP - 371
EP - 386
JO - Nutrition, Metabolism and Cardiovascular Diseases
JF - Nutrition, Metabolism and Cardiovascular Diseases
SN - 0939-4753
IS - 5
ER -