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Recent evidence provides the basis for this model proposing a role for apoA-I in cellular metabolism. Lipid-poor apoA-I is produced during remodeling of HDL and is known to be internalized by cells (possibly involving a receptor yet unidentified). HDL and apoA-I activate PKC through a pathway possibly involving PC and PI hydrolysis, and treatment with apoA-I stimulates several downstream events in some cells including phosphorylation of cell proteins, inhibition of apoptosis, and stimulation of mitogenic pathways. (See Fidge, p. 187.)
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Copyright © 2003 by Lipid Research, Inc.
