MicroRNAs regulating oxidative stress and inflammation in relation to obesity and atherosclerosis.
A primary event in atherogenesis is the infiltration of activated inflammatory cells into the arterial wall. There they secrete reactive oxygen species and oxidize lipoproteins, inducing foam cell formation and endothelial cell apoptosis, which in turn lead to plaque growth, erosion, and rupture. In addition, there is evidence that this vicious circle between oxidative stress and inflammation occurs not only in the diseased arterial wall but also in adipose tissues in obesity. In this condition, oxidative stress and inflammation impair adipocyte maturation, resulting in defective insulin action and adipocytokine signaling. This observation raises questions regarding what molecules are probably common regulators of these pathogenic processes in adipose and vascular tissues. Candidates are small, noncoding, microRNAs (miRs) that control gene expression by inducing mRNA degradation or blocking translation. This review summarizes recent insights into the roles of miRs in regulation of oxidative stress and inflammation in vascular and adipose tissues. It emphasizes the role of miR-containing microvesicles in the interaction between inflammatory cells and endothelial cells within these tissues and in communication between these tissues, possibly explaining the similarity and the simultaneity of molecular changes and interactions in adipose and vascular tissues.-Hulsmans, M., De.[1]References
- MicroRNAs regulating oxidative stress and inflammation in relation to obesity and atherosclerosis. Hulsmans, M., De Keyzer, D., Holvoet, P. FASEB J. (2011) [Pubmed]
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