Abstract
This synopsis emphasizes the inappropriateness of a “single stimulus-single response” approach in understanding the response of the arterial wall to injury and repair. The outcome of any injurious stimulus is a series of interactive cascades among the endogenous and exogenous cellular and non-cellular components of the arterial wall, and the cellular and non-cellular elements of the blood. Both genetic and hemodynamic factors can further influence this response. The more prominent of the cellular and non-cellular components have been discussed. These include: 1) the vascular endothelium, its dynamic interaction with macromolecules and formed elements of the blood, its role in the transport of plasma proteins, its influence on the function of arterial smooth muscle cells and the recruitment of blood-born monocytes; 2) the arterial smooth muscle cell, its role in the vasomotor function of the artery wall, arterial repair and reconstruction, metabolism of lipids and the secretion of cytokines regulating monocyte recruitment; 3) the mononuclear phagocyte, its role in arterial debridement, metabolism of modified LDLs, a precursor of the cholesteryl ester-rich foam cell, and the secretion of neutral hydrolases, bioactive lipids and cytokines; 4) lymphocytes, as mediators of the inflammatory response and possible autoimmune reactions; 5) platelets, their roles in hemostasis, thrombosis, atherogenesis, and the repair process and 6) plasma LDLs, their oxidative modification by cells of the vessel wall and their roles in the injury process. The interactive processes among arterial and circulating components in both injury and repair is emphasized.