Abstract
Background and Aims: Smooth muscle cells (SMCs) accumulate into the intima during the process of atherosclerosis, where they switch from a contractile to a synthetic phenotype. We previously identified S100A4 as being a marker of the synthetic SMCs. Recently we have shown that extracellular S100A4 induces a pro-inflammatory-like SMC phenotype and is causally related to atherosclerotic plaque progression. Our aim is to study the role of intracellular S100A4 depletion in the SMC phenotypic transition during atherosclerosis.
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