This chapter addresses extrinsic signals that affect vascular smooth muscle cell (SMC) phenotype and intrinsic cellular and molecular processes that affect SMC activities during atherogenesis. SMCs participate in all stages of atheroma formation. In the intima, monocytes differentiate into macrophages that phagocytose modified lipids and lipoprotein particles and become foam cells. Cytokines and growth factors such as platelet-derived growth factor (PDGF)-BB released from macrophages and foam cells induce dedifferentiation and migration of SMCs from media to intima. SMCs are centrally involved in the progression from early fatty streak to advanced fibrofatty atheroma. Plaque stability becomes critical as atherosclerosis progresses. SMCs support plaque stability by synthesizing extracellular matrix (ECM) proteins, lending mechanical strength to the fibrous cap overlying the plaque. SMC death is also important, as loss of SMCs limits ECM synthesis. At basal levels, autophagy recycles damaged cellular components and promotes survival, and therefore may serve to stabilize atheromas.
- Atheroma progression
- Extracellular matrix (ECM)
- Plaque stability
- Platelet-derived growth factor (PDGF)
- Vascular smooth muscle cell (SMC)
ASJC Scopus subject areas
- Biochemistry, Genetics and Molecular Biology(all)