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Figure 2 Formation of the fibrofatty plaque. The transition from the fatty streak to the more fibrous lesion involves the migration of smooth muscle cells (SMCs) from the tunica media through the internal elastic lamina into the intima, where they secrete extracellular matrix molecules such as fibrillar collagen and elastin and can divide in response to mitogenic stimuli. The mononuclear phagocytes will imbibe modified lipoproteins such as oxidized low-density lipoprotein (LDL) through scavenger receptors to form foam cells. The activated mononuclear phagocytes in the lesions release chemoattractant cytokines, proinflammatory mediators including cytokines, and small lipid molecules such leukotrienes and prostaglandins, as well as reactive oxygen species (ROS). When SMCs encounter fibrogenic stimuli such as transforming growth factor-beta, they boost their production of extracellular matrix macromolecules, including fibrillar collagen, depicted by the triple helical structures in the diagram and elastin. OxLDL = oxidized low-density lipoprotein.
