Sustained arterial injury and progression of atherosclerosis.

In this paper the following findings were described: 1) Murine arteriosclerosis induced by immune challenge was ultrastructurally characterized by intimal monocyte-macrophage recruitment and minor endothelial alterations; 2) Atherosclerotic lesions of human coronary arteries exhibited frequently segmental or patchy neovascularization, probably representing a response to intimal injury as an example of repair process. Newly formed blood vessels in the intima were derived from both adventitial and luminal endothelial growth; 3) Angiogenesis in vitro was related to the activation of fibrinolytic system especially via the autocrine production of u-PA from endothelial cells, and this process was modulated by cytokines and TGF beta. These findings add more evidence for the hypothesis that the chronic inflammation-repair process plays an essential role in the initiation and progression of atherosclerosis.