Prof. Johannes Waltenberger,
Novel insights into how smooth muscle cells (SMCs) are controlled greatly adds to our current understanding of atherosclerosis and plaque stability.The most recent and most exciting new concepts on vascular smooth muscle cell biology were presented and discussed in a dedicated symposium here at the 2013 ESC Congress in Amsterdam.Smooth muscle cells (SMCs) are major components of the arterial wall, as well as of the fibrous cap of the advanced atherosclerotic lesion. It has been known for years that uncontrolled proliferation of these cells leads to atherosclerotic plaque progression and the formation of stenotic lesions. Dr. C. De Vries from Amsterdam, NL, argued in her lecture on nuclear receptors in SMCs, that a reduced proliferation rate is likely to be deleterious as well, as the stability of the fibrous cap will be reduced and plaque rupture facilitated. Altogether, the regulation of SMC proliferation is a tightly regulated process involving a complex molecular machinery. Dr. P. Bouchet from Strasbourg, FR, extended on this notion focussing on the role of LRP, a representative from the LDL-receptor family, which activates the so called Wnt5a pathway and can trigger vascular calcification using Sox9 and Cart1.The behaviour of SMC is closely related to their differentiation state, as Dr. M-L Bochaton-Piallat from Geneva (CH) elucidated. She convincingly introduced S100A4 and Calmodulin as novel targets to modify SMC differentiation, with S100A4-inhibitors as well as the W7Cam-inhibitor being promising candidate molecules. Finally, Dr. M Bennett from Cambridge, UK, elaborated on the role of bone-marrow-derived SMC progenitor cells in arterial remodelling.Previous methodology using the detection of differentiation markers resulted in conflicting data. We now know that this is not the way to go anymore, while the use of genetic tracking of cells allow us to safely identify their origin and moreover, provides a basis for selective ablation, thereby modifying the atherogenic process.
Smooth muscle cells: friend or foe in atherosclerosis?
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