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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.)

Spontaneous experimental atherosclerosis in hypercholesterolemic mice advances with ageing and correlates with mitochondrial reactive oxygen species

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Author(s):
Dorighello, Gabriel G. [1] ; Paim, Bruno A. [2] ; Leite, Ana Catarina R. [2] ; Vercesi, Anibal E. [2] ; Oliveira, Helena C. F. [1]
Total Authors: 5
Affiliation:
[1] Biol Inst, Dept Struct & Funct Biol, Campinas, SP - Brazil
[2] Univ Estadual Campinas, Fac Med Sci, Dept Clin Pathol, Campinas, SP - Brazil
Total Affiliations: 2
Document type: Journal article
Source: Experimental Gerontology; v. 109, n. SI, p. 47-50, AUG 2018.
Web of Science Citations: 6
Abstract

Ageing and atherosclerosis are associated with oxidative stress. Mitochondrial redox function declines with ageing. Here we tested whether ageing LDL receptor knockout mice (LDLr-/-) develop spontaneous atherosclerosis and whether mitochondria' reactive oxygen species (mtROS) correlate with atherosclerosis. Compared with young mice, aged LDLr-/- mice exhibited 20-fold larger aortic lesion size, although the plasma cholesterol levels did not vary between age groups. The lesion sizes increased exponentially from 3 to 24 months of age (r = 0.92, p = 0.0001) and were correlated with mtROS across the age range (r = 0.81, p = 0.0001). Thus, LDLr-/- mice develop spontaneous diet-independent atherosclerosis, that advances exponentially with ageing. We propose that age related increases in mtROS contribute to accelerate atherosclerosis development in hypercholesterolemic mice. (C) 2017 Elsevier Inc. All rights reserved. (AU)

FAPESP's process: 13/07607-8 - OCRC - Obesity and Comorbidities Research Center
Grantee:Licio Augusto Velloso
Support type: Research Grants - Research, Innovation and Dissemination Centers - RIDC
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