2 research outputs found
Age-associated murine cardiac lesions are attenuated by the mitochondria-targeted antioxidant SkQ1
Age-related changes in mammalian hearts
often result in cardiac hypertrophy and fibrosis that are
preceded by inflammatory infiltration. In this paper, we
show that lifelong treatment of BALB/c and C57BL/6
mice with the mitochondria-targeted antioxidant SkQ1
retards senescence-associated myocardial disease
(cardiomyopathy), cardiac hypertrophy, and diffuse
myocardial fibrosis. To investigate the molecular basis
of the action of SkQ1, we have applied DNA microarray
analysis. The global gene expression profile in heart
tissues was not significantly affected by administration
of SkQ1. However, we found some small but statistically
significant modifications of the pathways related to cellto-cell contact, adhesion, and leukocyte infiltration.
Probably, SkQ1-induced decrease in leukocyte and
mesenchymal cell adhesion and/or infiltration lead to a
reduction in age-related inflammation and subsequent
fibrosis. The data indicate a causative role of
mitochondrial reactive oxygen species in cardiovascular
aging and imply that SkQ1 has poteential as a drug
against age-related cardiac dysfunction