Correlation between Mitochondrial Reactive Oxygen and Severity of Atherosclerosis
Autor: | Bruno A. Paim, Gabriel G. Dorighello, Mônica Siqueira Ferreira, Samara Kiihl, Helena C. F. Oliveira, Rodrigo Ramos Catharino, Anibal E. Vercesi |
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Rok vydání: | 2016 |
Předmět: |
0301 basic medicine
Aging medicine.medical_specialty Article Subject Mitochondrial redox chemistry.chemical_element Mitochondria Liver Mitochondrion medicine.disease_cause Biochemistry Oxygen Cholesterol Synthesis Inhibition Correlation Lesion Mice 03 medical and health sciences Internal medicine Plasma lipids medicine Animals lcsh:QH573-671 Mice Knockout lcsh:Cytology business.industry Cell Biology General Medicine Atherosclerosis Cholesterol 030104 developmental biology Endocrinology chemistry medicine.symptom Reactive Oxygen Species business NADP Oxidative stress Research Article |
Zdroj: | Oxidative Medicine and Cellular Longevity Oxidative Medicine and Cellular Longevity, Vol 2016 (2016) |
ISSN: | 1942-0994 1942-0900 |
DOI: | 10.1155/2016/7843685 |
Popis: | 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. |
Databáze: | OpenAIRE |
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