[Experimental atherogenesis].
The arterial wall possesses homeostatic mechanisms which are fundamental to the maintenance of its anatomical and functional integrity. The relative or absolute insufficiency of such mechanisms can lead with time to vascular disease, not the least of which is atherosclerosis. The understanding of the physiology of the arterial wall seems therefore necessary to a better approach to the study of several pathological processes. Four cell types play a critical role in the response of the vascular wall to physiological and pathological stimuli. They are the endothelial cell, the smooth muscle cell, the monocyte/macrophage and the platelet. The ordered interaction among these cell types is responsible for the maintenance of vascular integrity and, thus, for an efficient arterial response to physiological stimuli. Thus, it can be conceptually said that atherosclerosis derives from an excessive biological response to pathological stimuli. The current knowledge on the properties and potential interactions among each of the cells present and interacting with the arterial wall in relation to physiological mechanisms and atherogenic stimuli is discussed.
D000818:Animals; D001158:Arteries / Q000473:pathology / Q000502:physiology; D001161:Arteriosclerosis / Q000209:etiology / Q000473:pathology; D001792:Blood Platelets / Q000502:physiology; D010856:Columbidae; D004195:Disease Models, Animal; D004727:Endothelium / Q000502:physiology; D000882:Haplorhini; D006706:Homeostasis; D006801:Humans; D008074:Lipoproteins / Q000378:metabolism; D008264:Macrophages / Q000502:physiology; D008855:Microscopy, Electron, Scanning; D009000:Monocytes / Q000502:physiology; D009131:Muscle, Smooth, Vascular / Q000473:pathology / Q000502:physiology; D010982:Platelet-Derived Growth Factor / Q000502:physiology; D011817:Rabbits; D013552:Swine
D008074:Lipoproteins; D010982:Platelet-Derived Growth Factor
Aterogenesi sperimentale.