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Sci. Signal., 17 March 2009
Vol. 2, Issue 62, p. ra11
[DOI: 10.1126/scisignal.2000143]


Editor's Summary

Akting on the Vasculature
Although obesity is a well-known risk factor for cardiovascular disease, the signals that connect the two remain unclear. Noting that aberrant signaling involving mammalian target of rapamycin (mTOR) and Akt has been linked to obesity and its pathophysiological complications and that both of these kinases have been implicated in development of cellular senescence, Wang et al. explored the roles of Akt and mTOR in endothelial cell senescence. They showed that increased endothelial Akt signaling linked a high-fat diet to increased endothelial cell senescence and vascular dysfunction in mice. Intriguingly, the mTOR inhibitor rapamycin inhibited the long-term activation of endothelial Akt, as well as vascular cell senescence, and ameliorated the vascular sequelae of ischemia. The authors thus propose that inhibition of Akt activation with rapamycin therapy may have clinical benefits in obesity-related cardiovascular disease.

Citation: C.-Y. Wang, H.-H. Kim, Y. Hiroi, N. Sawada, S. Salomone, L. E. Benjamin, K. Walsh, M. A. Moskowitz, J. K. Liao, Obesity Increases Vascular Senescence and Susceptibility to Ischemic Injury Through Chronic Activation of Akt and mTOR. Sci. Signal. 2, ra11 (2009).

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Adipose Tissue Endothelial Cells From Obese Human Subjects: Differences Among Depots in Angiogenic, Metabolic, and Inflammatory Gene Expression and Cellular Senescence.
A. Villaret, J. Galitzky, P. Decaunes, D. Esteve, M.-A. Marques, C. Sengenes, P. Chiotasso, T. Tchkonia, M. Lafontan, J. L. Kirkland, et al. (2010)
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