[New concepts of atherogenesis].
The main advances since 1980 in our understanding of atherosclerosis can be summarised under four headings. 1) The migration and proliferation of smooth muscle cells from the media into the intima are key-events of atherogenesis, and probably also of restenosis following percutaneous transluminal coronary angioplasty. The experimental study of their regulations, especially looking for inhibitors, has therefore gained increased interest as it may provide original approaches to the prevention of post-angioplasty restenosis. 2) The histiocytes/macrophages, derived from blood monocytes, also take a major part in the initiation of atherosclerotic lesions. An intensive research activity is now being devoted to elucidating the many facets of their participation in atherogenesis. 3) Brown and Goldstein's discoveries have explained the biochemical mechanisms of the increased plasma low-density lipoprotein (LDL) concentration found in familial hypercholesterolemia (type IIa), although they did not completely solve the enigma of lipid deposition in the arterial wall. The metabolic handling of modified LDLs appears to be crucial to the foamy transformation of macrophages and, possibly, of smooth muscle cells. 4) Risk factors identified by epidemiology are usually held responsible for atherosclerosis. Yet this causal interpretation is not entirely satisfactory, and alternative or complementary hypotheses are being but forward. Among them, the most consistent submits that a viral aggression of the arterial wall is involved in the genesis and progression of atherosclerosis.
Capron
L
L
Centre de recherches sur les maladies vasculaires périphériques, Hôpital Broussais, Paris.
D000800:Angioplasty, Balloon / Q000009:adverse effects; D001158:Arteries / Q000378:metabolism; D001161:Arteriosclerosis / Q000453:epidemiology / Q000209:etiology*; D002455:Cell Division; D002465:Cell Movement; D006566:Herpesviridae Infections / Q000150:complications; D006801:Humans; D050356:Lipid Metabolism; D008077:Lipoproteins, LDL / Q000378:metabolism; D008264:Macrophages / Q000502:physiology; D009131:Muscle, Smooth, Vascular / Q000473:pathology
D008077:Lipoproteins, LDL
Notions nouvelles sur l'athérogenèse.