Correlation between Mitochondrial Reactive Oxygen and Severity of AtherosclerosisReport as inadecuate

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Oxidative Medicine and Cellular Longevity - Volume 2016 2016, Article ID 7843685, 10 pages -

Research Article

Department of Structural and Functional Biology, Biology Institute, State University of Campinas, 13083-862 Campinas, SP, Brazil

Department of Clinical Pathology, Faculty of Medical Sciences, State University of Campinas, 13083-887 Campinas, SP, Brazil

Department of Statistics, Institute of Mathematics, Statistic and Scientific Computation, State University of Campinas, 13083-859 Campinas, SP, Brazil

Received 24 April 2015; Revised 7 June 2015; Accepted 22 June 2015

Academic Editor: Celia Quijano

Copyright © 2016 Gabriel G. Dorighello et al. 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.


Atherosclerosis has been associated with mitochondria dysfunction and damage. Our group demonstrated previously that hypercholesterolemic mice present increased mitochondrial reactive oxygen mtROS generation in several tissues and low NADPH-NADP+ ratio. Here, we investigated whether spontaneous atherosclerosis in these mice could be modulated by treatments that replenish or spare mitochondrial NADPH, named citrate supplementation, cholesterol synthesis inhibition, or both treatments simultaneously. Robust statistical analyses in pooled group data were performed in order to explain the variation of atherosclerosis lesion areas as related to the classic atherosclerosis risk factors such as plasma lipids, obesity, and oxidative stress, including liver mtROS. Using three distinct statistical tools univariate correlation, adjusted correlation, and multiple regression with increasing levels of stringency, we identified a novel significant association and a model that reliably predicts the extent of atherosclerosis due to variations in mtROS. Thus, results show that atherosclerosis lesion area is positively and independently correlated with liver mtROS production rates. Based on these findings, we propose that modulation of mitochondrial redox state influences the atherosclerosis extent.

Author: Gabriel G. Dorighello, Bruno A. Paim, Samara F. Kiihl, Mônica S. Ferreira, Rodrigo R. Catharino, Anibal E. Vercesi, and Hel



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