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1.
Arch Cardiol Mex ; 71(3): 241-9, 2001.
Artigo em Espanhol | MEDLINE | ID: mdl-11665662

RESUMO

We describe tumour necrosis factor alpha and its role in the development of the atherosclerotic lesion, and detail the effects of this cytokine upon vascular endothelial cells under normal and high risk conditions. We propose that TNF-alpha performs a central role in the progression of the lesion since, once the endothelial cell feedback regulatory mechanisms are altered, there is an increase in the microenvironment TNF-alpha concentration, which together with some of the already well known risk factors, generates an environment that favours and perpetuates the development of the atheromatous lesion.


Assuntos
Arteriosclerose/etiologia , Fator de Necrose Tumoral alfa/fisiologia , Endotélio Vascular/fisiologia , Humanos
2.
Gac Med Mex ; 137(4): 335-45, 2001.
Artigo em Espanhol | MEDLINE | ID: mdl-11519357

RESUMO

Cardiovascular disease is the leading cause of mortality in Mexico, as well as in other Western countries. Conventional risk factors for atherosclerosis, such as cigarette smoking, systemic hypertension, diabetes mellitus, and hypercholesterolemia, do not explain this association completely. Recently, it has been recognized that hyperhomocysteinemia contributes to the atherosclerotic process, promoting endothelial damage and oxidative stress in the vascular wall. Homocysteine, an amino acid generated under physiologic conditions after ingestion of protein-rich foods, is used in a variety of metabolic pathways. Elevated plasma levels of this amino acid (higher than 15 mmol/L or lower in the presence of other cardiovascular risk factors) promote the development of atherosclerosis. Folic acid and vitamin B6 and B12 supplements decrease plasma levels of homocysteine effectively and may play an important role in the prevention and treatment of atherosclerotic vascular disease.


Assuntos
Doença das Coronárias/etiologia , Hiper-Homocisteinemia/complicações , Doença da Artéria Coronariana/etiologia , Homocisteína/fisiologia , Humanos , Hiper-Homocisteinemia/diagnóstico , Hiper-Homocisteinemia/tratamento farmacológico , Fatores de Risco , Trombose/etiologia
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