ArticleOxidative medicine and cellular longevity2016
Correlation between Mitochondrial Reactive Oxygen and Severity of Atherosclerosis.
Article in Oxidative medicine and cellular longevity, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed.
- The perspective of modern transplant science - transplant arteriosclerosis: inspiration derived from mitochondria associated endoplasmic reticulum membrane dysfunction in arterial diseases.International journal of surgery (London, England) · 2025Review
- Is L-Arginine an Appropriate Alternative for Conventional Anti-Atherosclerotic Therapy?: A Comprehensive Review.Health science reports · 2025Article
- NADPCurrent medicinal chemistry · 2025Review
- Role of ROS and autophagy in the pathological process of atherosclerosis.Journal of physiology and biochemistry · 2024Review
- A dual Keap1 and p47Cell death & disease · 2022Article
- Mild Mitochondrial Uncoupling Decreases Experimental Atherosclerosis, A Proof of Concept.Journal of atherosclerosis and thrombosis · 2022Article
- Puerarin Attenuates LPS-Induced Inflammatory Responses and Oxidative Stress Injury in Human Umbilical Vein Endothelial Cells through Mitochondrial Quality Control.Oxidative medicine and cellular longevity · 2021Article
- Molecular Dysfunctions of Mitochondria-Associated Endoplasmic Reticulum Contacts in Atherosclerosis.Oxidative medicine and cellular longevity · 2021Review
- Endothelial dysfunction in neuroprogressive disorders-causes and suggested treatments.BMC medicine · 2020Review
- SIRT3-mediated deacetylation of PRDX3 alleviates mitochondrial oxidative damage and apoptosis induced by intestinal ischemia/reperfusion injury.Redox biology · 2020Article
- The impact of dyslipidemia and oxidative stress on vasoactive mediators in patients with renal dysfunction.International urology and nephrology · 2019Review
- Role of pyroptosis in cardiovascular disease.Cell proliferation · 2019Review
- Activating the PGC-1Oxidative medicine and cellular longevity · 2018Article
- Protective Role of Perivascular Adipose Tissue in Endothelial Dysfunction and Insulin-Induced Vasodilatation of Hypercholesterolemic LDL Receptor-Deficient Mice.Frontiers in physiology · 2018Article
- In vitro and in vivo evaluation of the toxicities induced by metallic nickel nano and fine particles.Journal of molecular histology · 2016Article
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
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.
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