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Plasma proteomic analysis of stable coronary artery disease indicates impairment of reverse cholesterol pathway

Coronary artery disease (CAD) is one of the largest causes of death worldwide yet the traditional risk factors, although useful in identifying people at high risk, lack the desired predictive accuracy. Techniques like quantitative plasma proteomics holds immense potential to identify newer markers a...

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Autores principales: Basak, Trayambak, Tanwar, Vinay Singh, Bhardwaj, Gourav, Bhardwaj, Nitin, Ahmad, Shadab, Garg, Gaurav, V, Sreenivas, Karthikeyan, Ganesan, Seth, Sandeep, Sengupta, Shantanu
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4923873/
https://www.ncbi.nlm.nih.gov/pubmed/27350024
http://dx.doi.org/10.1038/srep28042
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author Basak, Trayambak
Tanwar, Vinay Singh
Bhardwaj, Gourav
Bhardwaj, Nitin
Ahmad, Shadab
Garg, Gaurav
V, Sreenivas
Karthikeyan, Ganesan
Seth, Sandeep
Sengupta, Shantanu
author_facet Basak, Trayambak
Tanwar, Vinay Singh
Bhardwaj, Gourav
Bhardwaj, Nitin
Ahmad, Shadab
Garg, Gaurav
V, Sreenivas
Karthikeyan, Ganesan
Seth, Sandeep
Sengupta, Shantanu
author_sort Basak, Trayambak
collection PubMed
description Coronary artery disease (CAD) is one of the largest causes of death worldwide yet the traditional risk factors, although useful in identifying people at high risk, lack the desired predictive accuracy. Techniques like quantitative plasma proteomics holds immense potential to identify newer markers and this study (conducted in three phases) was aimed to identify differentially expressed proteins in stable CAD patients. In the first (discovery) phase, plasma from CAD cases (angiographically proven) and controls were subjected to iTRAQ based proteomic analysis. Proteins found to be differentially expressed were then validated in the second and third (verification and validation) phases in larger number of (n = 546) samples. After multivariate logistic regression adjusting for confounding factors (age, diet, etc.), four proteins involved in the reverse cholesterol pathway (Apo A1, ApoA4, Apo C1 and albumin) along with diabetes and hypertension were found to be significantly associated with CAD and could account for approximately 88% of the cases as revealed by ROC analysis. The maximum odds ratio was found to be 6.70 for albumin (p < 0.0001), followed by Apo AI (5.07, p < 0.0001), Apo CI (4.03, p = 0.001), and Apo AIV (2.63, p = 0.003). Down-regulation of apolipoproteins and albumin implicates the impairment of reverse cholesterol pathway in CAD.
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spelling pubmed-49238732016-06-28 Plasma proteomic analysis of stable coronary artery disease indicates impairment of reverse cholesterol pathway Basak, Trayambak Tanwar, Vinay Singh Bhardwaj, Gourav Bhardwaj, Nitin Ahmad, Shadab Garg, Gaurav V, Sreenivas Karthikeyan, Ganesan Seth, Sandeep Sengupta, Shantanu Sci Rep Article Coronary artery disease (CAD) is one of the largest causes of death worldwide yet the traditional risk factors, although useful in identifying people at high risk, lack the desired predictive accuracy. Techniques like quantitative plasma proteomics holds immense potential to identify newer markers and this study (conducted in three phases) was aimed to identify differentially expressed proteins in stable CAD patients. In the first (discovery) phase, plasma from CAD cases (angiographically proven) and controls were subjected to iTRAQ based proteomic analysis. Proteins found to be differentially expressed were then validated in the second and third (verification and validation) phases in larger number of (n = 546) samples. After multivariate logistic regression adjusting for confounding factors (age, diet, etc.), four proteins involved in the reverse cholesterol pathway (Apo A1, ApoA4, Apo C1 and albumin) along with diabetes and hypertension were found to be significantly associated with CAD and could account for approximately 88% of the cases as revealed by ROC analysis. The maximum odds ratio was found to be 6.70 for albumin (p < 0.0001), followed by Apo AI (5.07, p < 0.0001), Apo CI (4.03, p = 0.001), and Apo AIV (2.63, p = 0.003). Down-regulation of apolipoproteins and albumin implicates the impairment of reverse cholesterol pathway in CAD. Nature Publishing Group 2016-06-28 /pmc/articles/PMC4923873/ /pubmed/27350024 http://dx.doi.org/10.1038/srep28042 Text en Copyright © 2016, Macmillan Publishers Limited http://creativecommons.org/licenses/by/4.0/ This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/
spellingShingle Article
Basak, Trayambak
Tanwar, Vinay Singh
Bhardwaj, Gourav
Bhardwaj, Nitin
Ahmad, Shadab
Garg, Gaurav
V, Sreenivas
Karthikeyan, Ganesan
Seth, Sandeep
Sengupta, Shantanu
Plasma proteomic analysis of stable coronary artery disease indicates impairment of reverse cholesterol pathway
title Plasma proteomic analysis of stable coronary artery disease indicates impairment of reverse cholesterol pathway
title_full Plasma proteomic analysis of stable coronary artery disease indicates impairment of reverse cholesterol pathway
title_fullStr Plasma proteomic analysis of stable coronary artery disease indicates impairment of reverse cholesterol pathway
title_full_unstemmed Plasma proteomic analysis of stable coronary artery disease indicates impairment of reverse cholesterol pathway
title_short Plasma proteomic analysis of stable coronary artery disease indicates impairment of reverse cholesterol pathway
title_sort plasma proteomic analysis of stable coronary artery disease indicates impairment of reverse cholesterol pathway
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4923873/
https://www.ncbi.nlm.nih.gov/pubmed/27350024
http://dx.doi.org/10.1038/srep28042
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