Atherosclerosis is a disease affecting the arterial blood vessel. It is commonly referred to as a "hardening" or "furring" of the arteries. It is caused by the formation of multiple plaques within the arteries.

Pathologically, the atheromatous plaque is divided into three distinct components:

1. The atheroma ("lump of porridge", from Athera, porridge in Greek,) is the nodular accumulation of a soft, flaky, yellowish material at the center of large plaques, composed of macrophages nearest the lumen of the artery, sometimes with
2. Underlying areas of cholesterol crystals, and possibly also
3. Calcification at the outer base of older/more advanced lesions.

The following terms are similar, yet distinct, in both spelling and meaning, and can be easily confused: arteriosclerosis, arteriolosclerosis and atherosclerosis. Arteriosclerosis, is a general term describing any hardening (and loss of elasticity) of medium or large arteries (in Latin, Arterio meaning artery and sclerosis meaning hardening), arteriolosclerosis is arteriosclerosis mainly affecting the arterioles (small arteries), atherosclerosis is a hardening of an artery specifically due to an atheromatous plaque (in Latin Athero means porrige-like). Therefore, atherosclerosis is a form of arteriosclerosis.

More on [ Atherosclerosis ]

Arteriosclerosis, Thrombosis, and Vascular Biology current issue

What is Truth? Standards of Scientific Integrity in American Heart Association Journals [Editorials]
Miano, J. M.
The Fibronectin RGD Motif Is Required for Multiple Angiogenic Events During Early Embryonic Development [Retraction]
Takahashi, S., Moser, M., Montanez, E., Nakano, T., Seo, M., Backert, S., Inoue, I., Awata, T., Katayama, S., Komoda, T., Fassler, R. In the present study we demonstrated that inactivation of the RGD motif in mice results in a severe circulation defect that differs from the defect seen in mice lacking FN. Our findings indicate that FN is essential for both vasculogenesis and angiogenesis, and the RGD motif plays specific roles in angiogenesis.
Lipolysis Needed for Chylomicron Uptake? [Editorials]
Parthasarathy, S. Despite clinical evidence that postprandial lipemia and chylomicrons could contribute to atherosclerosis, direct evidence is lacking. The study by Weinstein et al1 provides evidence to suggest that intact chylomicrons might be atherogenic by using genetically altered mice lacking Gpihbp1 protein, which may play a major role in the lipolysis of triglyceride-rich lipoproteins. However, the study does not rule out a contribution by remnants or limited lipolysis by other potential enzymes or pathways. It might be intriguing to determine the contribution of cholesterol derivatives in the chylomicrons to the lesions and the nature of the lesions.
Smoking Out the Cause of Thrombosis [Editorials]
Campbell, R. A., Machlus, K. R., Wolberg, A. S.
Triglyceride-Rich Lipoproteins and Plasma Lipid Transport [History of Discovery]
Havel, R. J. This memoir provides a history of the triglyceride-rich lipoproteins of blood plasma over the last half-century. As precursors of low-density lipoproteins and in their own right, triglyceride-rich lipoproteins are essential to the formation of atherosclerotic plaques and to consequent ischemic vascular disease. The author recounts research at the National Heart Institute during 1953 to 1956 and continuing thereafter at the University of California San Francisco. Emphasis is placed on key insights arising from investigations of human disease, the interplay of fatty acid and triglyceride-transport involving the liver, small intestine, adipose tissue and muscle, and the role of the liver in the synthesis and catabolism of atherogenic lipoproteins.
Chylomicronemia Elicits Atherosclerosis in Mice--Brief Report [Integrative Physiology/Experimental Medicine]
Weinstein, M. M., Yin, L., Tu, Y., Wang, X., Wu, X., Castellani, L. W., Walzem, R. L., Lusis, A. J., Fong, L. G., Beigneux, A. P., Young, S. G. Objective— The risk of atherosclerosis in the setting of chylomicronemia has been a topic of debate. In this study, we examined susceptibility to atherosclerosis in Gpihbp1-deficient mice (Gpihbp1–/–), which manifest severe chylomicronemia as a result of defective lipolysis. Methods and Results— Gpihbp1–/– mice on a chow diet have plasma triglyceride and cholesterol levels of 2812±209 and 319±27 mg/dL, respectively. Even though nearly all of the lipids were contained in large lipoproteins (50 to 135 nm), the mice developed progressive aortic atherosclerosis. In other experiments, we found that both Gpihbp1-deficient "apo-B48–only" mice and Gpihbp1-deficient "apo-B100–only" mice manifest severe chylomicronemia. Thus, GPIHBP1 is required for the processing of both apo-B48– and apo-B100–containing lipoproteins. Conclusions— Chylomicronemia causes atherosclerosis in mice. Also, we found that GPIHBP1 is required for the lipolytic processing of both apo-B48– and apo-B100–containing lipoproteins.

Subscribe to Atherosclerosis RSS feed