Article

Download article 		Title: Correlation between Mitochondrial Reactive Oxygen and Severity of Atherosclerosis
Author: Dorighello, Gabriel G.; Paim, Bruno A.; Kiihl, Samara F.; Ferreira, Mônica S.; Catharino, Rodrigo R.; Vercesi, Anibal E.; Oliveira, Helena C. F.
Year: 2016
Is part of: Oxidative Medicine and Cellular Longevity, v. 2016, p. 1 - 10
DOI: https://doi.org/10.1155/2016/7843685

Citation: Dorighello, Gabriel G.; Paim, Bruno A.; Kiihl, Samara F.; Ferreira, Mônica S.; Catharino, Rodrigo R.; Vercesi, Anibal E.; Oliveira, Helena C. F.; Correlation between Mitochondrial Reactive Oxygen and Severity of Atherosclerosis. Oxidative Medicine and Cellular Longevity, v.2016, p. 1-10, 2016

Abstract: 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.

Keywords: atherosclerosis; mitochondria; reactive oxigen species;
Subjects: CIENCIAS_DA_SAUDE; Saúde Pública; Lípides e Lipoproteínas; CIENCIAS_BIOLOGICAS; Bioquímica; Metabolismo e Bioenergética; Bioenergética Mitocondrial;

Funding: This study was supported by grants obtained by Helena C. F. Oliveira and Anibal E. Vercesi from the Brazilian agencies: Fundacao de Amparo a Pesquisa do Estado de Sao Paulo (FAPESP # 2011/50400-0 and 2011/51349-8) and Conselho Nacional de Desenvolvimento Cientifico e Tecnologico (CNPq). Gabriel G. Dorighello and Bruno A. Paim were supported by CNPq and FAPESP fellowships, respectively. The authors thank Ms. Natalia Mayumi Inada, Edilene de Souza Siqueira Santos, and Gabriela C. Tonini for the technical assistance. 		Financed by: