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Coordinación General de Investigación de la Facultad de Salud Pública y Nutrición y la Dirección General de Sistemas e Informática de la Universidad Autónoma de Nuevo León

2008, Number 4

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Rev Salud Publica Nutr 2008; 9 (4)

Aterogenesis

Arce-Torres MA, Haro AME, Ponce PLG, Núñez SAA, Ruiz-Esparza CJ, Robinson NOM

Language: Spanish
References: 39
Page:
PDF size: 261.89 Kb.


ABSTRACT

Human atherosclerosis is a multifactorial, pathological complex process, including two tightly related phenomena: atherosis, characterized for intracellular or extracellular lipid accumulation and also include foaming cells and inflammatory reaction; and hardening scare of the arterial wall caused by increased number of myocyte, dystrophy of extracellular matrix, calcification, necrobiosis and increased inflammatory reaction. Maybe the endothelium is the biggest organ of the body with endocrine, autocrine and paracrine. Realizes many functions like regulation of interchange of molecules between blood and vascular wall, also regulates vascular tone through nitric oxide and prostaglandin I2 causing relaxation of vascular smooth muscle, as well as development antithrombotic-fibrinolytic functions. A fundamental factor in atherosclerosis is the endothelial disfunction, a principal aspect in the nitric oxide reduction, probably caused by increased metabolic degradation or reduced synthesis. Besides is very important the role of low density lipoproteins (LDL), that in condition of endothelial disfunction remain a longer time in the subendothelial space and here are oxidized (modified), originating modified mimically LDL (MM-LDL). The cells that directly participate in the atheromatous plaque formation are the monocytes, which become in macrophages during maturation. By other side the MM-LDL are exposed to a broad oxidation and can stimulate or activate the macrophage, these cells do not have a mechanism to block the cholesterol uptake and poorly degrade the oxidized LDL. As a consequence of the uncontrolled cholesterol uptake the macrophage becomes to a foaming cell conducing to the cell death, the released lipids will create the atheromatous nucleus and toxic substances, which will injury the endothelium, that will progress from a dysfunctional endothelium to a damaged endothelium, showing some disappeared or destroyed regions. The exposure of this unfunctional endothelium to the underlying collagen blood, stimulate the platelet adherence, that together with the macrophages secrete grow factors, that stimulate proliferation and migration of smooth muscle cells of the medium layer.


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