Dysfunctional HDL as a Diagnostic and Therapeutic Target

The atheroprotective effects of HDL are mediated by several mechanisms, including its role in reverse cholesterol transport and via its antiinflammatory properties. However, not all HDL is functionally similar. HDL and apolipoprotein A-I may become dysfunctional or even proinflammatory and thus prom...

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Published inArteriosclerosis, thrombosis, and vascular biology Vol. 30; no. 2; pp. 151 - 155
Main Author Smith, Jonathan D.
Format Journal Article
LanguageEnglish
Published United States American Heart Association, Inc 01.02.2010
Subjects
Animals
Apolipoprotein A-I - metabolism
Atherosclerosis - diagnosis
Atherosclerosis - drug therapy
Atherosclerosis - metabolism
Biomarkers - metabolism
Cholesterol - metabolism
Humans
Hypolipidemic Agents - therapeutic use
Inflammation - diagnosis
Inflammation - drug therapy
Inflammation - metabolism
Lipoproteins, HDL - metabolism
Peroxidase - metabolism
Predictive Value of Tests
Protein Conformation
Protein Processing, Post-Translational
Structure-Activity Relationship
Online AccessGet full text
ISSN1079-5642
1524-4636
1524-4636
DOI10.1161/ATVBAHA.108.179226

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Abstract The atheroprotective effects of HDL are mediated by several mechanisms, including its role in reverse cholesterol transport and via its antiinflammatory properties. However, not all HDL is functionally similar. HDL and apolipoprotein A-I may become dysfunctional or even proinflammatory and thus promote atherosclerosis. ApoAI posttranslational modification can have a large impact on its function. Myeloperoxidase modification of apoAI impairs its function as a cholesterol acceptor, and the molecular changes induced by myeloperoxidase have been studied in detail. These studies provide the basis for the development of an oxidant-resistant form of apoAI and clinical measures of HDL modification and dysfunction, which may be useful as a treatment criterion.
AbstractList The atheroprotective effects of HDL are mediated by several mechanisms, including its role in reverse cholesterol transport and via its antiinflammatory properties. However, not all HDL is functionally similar. HDL and apolipoprotein A-I may become dysfunctional or even proinflammatory and thus promote atherosclerosis. ApoAI posttranslational modification can have a large impact on its function. Myeloperoxidase modification of apoAI impairs its function as a cholesterol acceptor, and the molecular changes induced by myeloperoxidase have been studied in detail. These studies provide the basis for the development of an oxidant-resistant form of apoAI and clinical measures of HDL modification and dysfunction, which may be useful as a treatment criterion.The atheroprotective effects of HDL are mediated by several mechanisms, including its role in reverse cholesterol transport and via its antiinflammatory properties. However, not all HDL is functionally similar. HDL and apolipoprotein A-I may become dysfunctional or even proinflammatory and thus promote atherosclerosis. ApoAI posttranslational modification can have a large impact on its function. Myeloperoxidase modification of apoAI impairs its function as a cholesterol acceptor, and the molecular changes induced by myeloperoxidase have been studied in detail. These studies provide the basis for the development of an oxidant-resistant form of apoAI and clinical measures of HDL modification and dysfunction, which may be useful as a treatment criterion.
The atheroprotective effects of HDL are mediated by several mechanisms, including its role in reverse cholesterol transport and via its antiinflammatory properties. However, not all HDL is functionally similar. HDL and apolipoprotein A-I may become dysfunctional or even proinflammatory and thus promote atherosclerosis. ApoAI posttranslational modification can have a large impact on its function. Myeloperoxidase modification of apoAI impairs its function as a cholesterol acceptor, and the molecular changes induced by myeloperoxidase have been studied in detail. These studies provide the basis for the development of an oxidant-resistant form of apoAI and clinical measures of HDL modification and dysfunction, which may be useful as a treatment criterion.
The atheroprotective effects of HDL are mediated by several mechanisms, including its role in reverse cholesterol transport and via its antiinflammatory properties. However, not all HDL is functionally similar. HDL and apolipoprotein A-I may become dysfunctional or even proinflammatory and thus promote atherosclerosis. ApoAI posttranslational modification can have a large impact on its function. Myeloperoxidase modification of apoAI impairs its function as a cholesterol acceptor, and the molecular changes induced by myeloperoxidase have been studied in detail. These studies provide the basis for the development of an oxidant-resistant form of apoAI and clinical measures of HDL modification and dysfunction, which may be useful as a treatment criterion. HDL-cholesterol is the “good cholesterol” because of its reverse cholesterol transport and antiinflammatory activities. However, HDL and apolipoprotein A-I can lose their protective activities through changes in protein or lipid composition as well as protein modifications. Assays for dysfunctional HDL could potentially be used as a criterion for preventative therapy.
The atheroprotective effects of HDL are mediated by several mechanisms including its role in reverse cholesterol transport and via its anti-inflammatory properties. However, not all HDL is functionally similar. HDL and apolipoprotein A-I may become dysfunctional or even pro-inflammatory, and thus promote atherosclerosis. ApoAI post-translational modification can have a large impact on its function. Myeloperoxidase modification of apoAI impairs it function as a cholesterol acceptor, and the molecular changes induced by myeloperoxidase have been studied in detail. These studies provide the basis for the development of an oxidant resistant form of apoAI and clinical measures of HDL modification and dysfunction, which may be useful as a treatment criterion.
Author Smith, Jonathan D.
AuthorAffiliation From the Department of Cell Biology, Cleveland Clinic, Ohio
AuthorAffiliation_xml – name: From the Department of Cell Biology, Cleveland Clinic, Ohio
Author_xml – sequence: 1
  givenname: Jonathan
  surname: Smith
  middlename: D.
  fullname: Smith, Jonathan D.
  organization: From the Department of Cell Biology, Cleveland Clinic, Ohio
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Snippet The atheroprotective effects of HDL are mediated by several mechanisms, including its role in reverse cholesterol transport and via its antiinflammatory...
The atheroprotective effects of HDL are mediated by several mechanisms including its role in reverse cholesterol transport and via its anti-inflammatory...
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SubjectTerms Animals
Apolipoprotein A-I - metabolism
Atherosclerosis - diagnosis
Atherosclerosis - drug therapy
Atherosclerosis - metabolism
Biomarkers - metabolism
Cholesterol - metabolism
Humans
Hypolipidemic Agents - therapeutic use
Inflammation - diagnosis
Inflammation - drug therapy
Inflammation - metabolism
Lipoproteins, HDL - metabolism
Peroxidase - metabolism
Predictive Value of Tests
Protein Conformation
Protein Processing, Post-Translational
Structure-Activity Relationship
Title Dysfunctional HDL as a Diagnostic and Therapeutic Target
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https://www.ncbi.nlm.nih.gov/pubmed/19679832
https://www.proquest.com/docview/733613515
https://pubmed.ncbi.nlm.nih.gov/PMC2809786
Volume 30
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