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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

Correlation between Mitochondrial Reactive Oxygen and Severity of Atherosclerosis

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Dorighello, Gabriel G. [1] ; Paim, Bruno A. [2] ; Kiihl, Samara F. [3] ; Ferreira, Monica S. [2] ; Catharino, Rodrigo R. [2] ; Vercesi, Anibal E. [2] ; Oliveira, Helena C. F. [1]
Total Authors: 7
[1] Univ Estadual Campinas, Inst Biol, Dept Struct & Funct Biol, BR-13083862 Campinas, SP - Brazil
[2] Univ Estadual Campinas, Fac Med Sci, Dept Clin Pathol, BR-13083887 Campinas, SP - Brazil
[3] Univ Estadual Campinas, Inst Math Stat & Sci Computat, Dept Stat, BR-13083859 Campinas, SP - Brazil
Total Affiliations: 3
Document type: Journal article
Web of Science Citations: 7

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. (AU)

FAPESP's process: 11/50400-0 - Mitochondrial energy metabolism, redox state and functionality in cell death and cardiometabolic and neurodegenerative disorders
Grantee:Aníbal Eugênio Vercesi
Support type: Research Projects - Thematic Grants