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. Author manuscript; available in PMC: 2010 May 10.
Published in final edited form as: Annu Rev Pathol. 2010;5:253–295. doi: 10.1146/annurev.pathol.4.110807.092250

Figure 8.

Figure 8

The role of SIRT1 in protection from atherosclerosis and cardiovascular disease (CVD). In the normal progression of atherosclerosis, damage and inflammation of blood vessel walls promote the infiltration of macrophages, where they take up and accumulate oxidized low-density lipoprotein, becoming foam cells that can eventually rupture and promote additional inflammation and plaque formation, which in turn occludes blood flow. Overexpression of SIRT1 in endothelial cells or treatment of mice with resveratrol SIRT1 reduces reactive oxygen species in vessel walls and slows the progression of CVD, apparently through multiple mechanisms. These include the suppression of inflammation by increasing endothelial nitric oxide synthase (eNOS) and decreasing nuclear factor kappa B (NF-κB) activity. Increased retrograde cholesterol transport in macrophages may also be a contributing factor. Abbreviations: cGMP, cyclic guanosine monophosphate; ICAM, intercellular adhesion molecule 1; IL-6, interleukin-6; iNOS, inducible NO, nitric oxide synthase; TNFα, tumor necrosis factor alpha.