Fig. 3.

Roles of HDACs in modulating hemodynamics-regulated EC dysfunctions, including proliferation, inflammation, and oxidation. Pro-atherogenic OS induces expression and nuclear accumulation of both class I (HDAC-1, − 2, and -3) and class II HDACs (HDAC-5 and -7). Moreover, OS further enhances the formation of HDAC-1/HDAC-2/HDAC-3 and HDAC-3/HDAC-5/HDAC-7 heterocomplexes to promote proliferation, inflammation, and oxidation. In contrast, atheroprotective PS induces phosphorylation-dependent nuclear export of class II HDACs to decrease HDAC levels in the nucleus to inhibit their effects on proliferation, inflammation, and oxidation. On the other hand, PS induces the expression of Class III (Sirt1) to enhance NO production