**4.2 HDL functions on vascular smooth muscle cells (VSMCs)**

Many stress factors could induce VSMCs shifting from a contractile phenotype to a synthetic phenotype, and consequently the activated VSMCs proliferate and migrate from the medial layer of vessels into the intima which results in neointimal hyperplasia and artery stenosis [79, 80]. HDL counterbalances the pro-inflammatory effects of ox-LDL by inhibiting intracellular reactive oxygen species (ROS) release and subsequent nuclear factor kappa-B (NF-κB) activation in VSMCs [81]. HDL also downregulates the production of fibroblast growth factor (FGF) and represses the proliferation of VSMCs triggered by ox-LDL [82]. HDL suppresses the expression of chemokines (CCL2, CCL5, CX3CL1, CCR2, and CX3CR1) and the proliferation of VSMCs induced by TNF-alpha via the SR-BI pathway [7]. In addition, HDL-associated alpha-antitrypsin (AAT) inhibits extracellular matrix degradation, cell detachment, and apoptosis triggered by elastase in human VSMCs [83].
