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

Tyrosine Sulfation of Leukocyte Adhesion Molecules and Chemokine Receptors Promotes Atherosclerosis [Editorials]
Koltsova, E., Ley, K.
Dimorphisms in the Membrane-Spanning Domain of EPCR Impact Systemic Coagulation [Editorials]
Esmon, C. T.
The Discovery of Cellular Immunity in the Atherosclerotic Plaque [History of Discovery]
Hansson, G. K., Jonasson, L. It is now generally accepted that atherosclerosis is an inflammatory/immune disease triggered by LDL accumulation in the artery wall. When discovering T cells and the molecular components of a cellular immune response, we proposed that atherosclerosis is an inflammatory process with an autoimmune component. This notion was met with general skepticism but has gained support from experimental and clinical studies. Here we describe some of the early studies that helped developing this concept.
The Molecular Mechanisms of HDL and Associated Vesicular Trafficking Mechanisms to Mediate Cellular Lipid Homeostasis [History of Discovery]
Schmitz, G., Grandl, M. HDL functions mainly as a cholesterol scavenger, facilitating transport of cholesterol to the liver for conversion to bile acids and secretion into the bile for elimination or recycling in the enterohepatic bile acid cycle. Because of its major function in cholesterol clearance, HDL is in general considered to be atheroprotective. From cell cholesterol can be removed by efflux especially to apoA-I and HDL as extracellular acceptors which transport the cholesterol to the liver for excretion. This process is called reverse cholesterol transport. In this context the ATP binding cassette transporter protein ABCA1 facilitates cellular cholesterol and phospholipid release to apoA-I-containing HDL precursors. In addition ABCA1 plays a role in vesicular lipid transport mechanisms required for HDL particle formation. In general to maintain intracellular lipid homeostasis, sterols and associated lipids move between cellular compartments by vesicular and nonvesicular pathways. However, cholesterol sorting on vesicle formation is poorly understood. This review summarizes the current knowledge of the molecular mechanisms of HDL and associated vesicular trafficking mechanisms to mediate cellular lipid homeostasis.
Adipose Tissue-Derived Stem Cells: Characterization and Potential for Cardiovascular Repair [Brief Reviews]
Madonna, R., Geng, Y.-J., De Caterina, R. Experimental studies have shown that cardiac transfer of unfractionated or partially purified bone marrow cells, as well as stem cells and progenitor cells derived from the bone marrow or peripheral blood, can enhance functional recovery after an acute myocardial infarction. However, the relatively low abundance, small tissue volume, difficult accessibility, and disease-related malfunction of bone marrow-derived stem cells hamper their clinical usefulness. Numerous studies have provided evidence that stromal cells derived from the adipose tissue (adipose tissue-derived stromal cells [ADSCs]) contain a population of adult multipotent mesenchymal stem cells and endothelial progenitor cells that can differentiate into several lineages, including endothelial cells, smooth muscle cells, and cardiomyocytes. The similarities between stem cells extracted from the bone marrow and the adipose tissue suggest the potential for the adipose tissue to act as an alternative, and perhaps preferable, cell source for repairing damaged tissues, such as the ischemic or infarcted heart. We have here reviewed the medical literature describing molecular and functional characterization, differentiation, potential role, and results obtained so far using ADSCs in tissue repair, with a particular focus on the role for ADSCs in cardiovascular repair and regeneration.
Lack of Tyrosylprotein Sulfotransferase Activity in Hematopoietic Cells Drastically Attenuates Atherosclerosis in Ldlr-/- Mice [Integrative Physiology/Experimental Medicine]
Westmuckett, A. D., Moore, K. L. Objective— Leukocyte recruitment is a major contributor in the development of atherosclerosis and requires a variety of proteins such as adhesion molecules, chemokines, and chemokine receptors. Several key molecular players implicated in this process are expressed on monocytes and require protein-tyrosine sulfation for optimal function in vitro, including human CCR2, CCR5, CX3CR1, and PSGL-1. We therefore hypothesized that protein-tyrosine sulfation in hematopoietic cells plays an important role in the development of atherosclerosis. Methods and Results— Lethally-irradiated Ldlr–/– mice were rescued with hematopoietic progenitors lacking tyrosylprotein sulfotransferase (TPST) activity attributable to deletion of the Tpst1 and Tpst2 genes. TPST deficient progenitors efficiently reconstituted hematopoiesis in Ldlr–/– recipients and transplantation had no effect on plasma lipids on a standard or atherogenic diet. However, we observed a substantial reduction in the size of atherosclerotic lesions and the number of macrophages in lesions from hyperlipidemic Ldlr–/– recipients transplanted with TPST deficient progenitors compared to wild-type progenitors. We also document for the first time that murine Psgl-1 and Cx3cr1 are tyrosine-sulfated. Conclusions— These data demonstrate that protein-tyrosine sulfation is an important contributor to monocytes/macrophage recruitment and/or retention in a mouse model of atherosclerosis.

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