Mouse Models of Experimental Atherosclerosis as a Tool for Checking a Putative Anti-Atherogenic Action of Drugs

Abstract

Studies concerning the pathogenesis of atherosclerosis entered a new phase at the turn of the 21st century. The 20th century was the age of cholesterol and lipoproteins, which has been concluded in a number of clinical studies carried out on a large scale, and they demonstrated unequivocally that normalization of hypercholesterolemia significantly decreased the incidence and mortality of coronary artery disease (Prevention of cardiovascular events and death with pravastatin in patients with coronary heart disease and a broad range of initial cholesterol levels. The Long-Term Intervention with Pravastatin in Ischaemic Disease (LIPID) Study Group. 1998; Scandinavian Simvastatin Survival Study Group. Randomised trial of cholesterol lowering in 4444 patients with coronary heart disease: The Scandinavian Simvastatin Survival Study (4S). 1994) Nearly to the end of the nineties, atherosclerosis had been assumed to develop as the so-called chronic response to injury (response-to-injury hypothesis) that resulted in the loss of endothelial cells which line the inner side of the vessels (Ross & Glomset, 1976). Atherosclerosis had been considered first of all a degenerative disease (Ross et al., 1977; Ross et al. 1984; Ross, 1986). However, approximately 20 years ago, the trials started to focus to a large extent on another pathogenetic mechanism of atherosclerosis, not considered so far – the inflammatory process.