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.
Sueishi
K
K
Department of Pathology, Faculty of Medicine, Kyushu University, Fukuoka, Japan.
Yasunaga
C
C
Castellanos
E
E
Kumamoto
M
M
Tanaka
K
K
D000818:Animals; D001158:Arteries / Q000473:pathology*; D001161:Arteriosclerosis / Q000209:etiology*; D002417:Cattle; D003324:Coronary Artery Disease / Q000209:etiology; D016207:Cytokines / Q000494:pharmacology; D005341:Fibrinolysin / Q000037:antagonists & inhibitors; D005342:Fibrinolysis; D006133:Growth Substances / Q000494:pharmacology; D006801:Humans; D007107:Immune System / Q000502:physiology*; D007249:Inflammation / Q000473:pathology*; D009389:Neovascularization, Pathologic; D010958:Plasminogen / Q000494:pharmacology
D016207:Cytokines; D006133:Growth Substances; D010958:Plasminogen; D005341:Fibrinolysin