Protein homocysteinylation and mechanisms of atherosclerosis

doi:10.7523/j.issn.2095-6134.2009.2.001

Abstract

Abstract:

Atherosclerosis is a world-wide disease with severe effects on human health. Although it remains unclear about the pathological mechanisms of atherosclerosis that can not be efficiently prevented and treated so far, a large body of evidence suggests that increased level of plasma homocysteine is an independent risk factor for atherosclerosis. Numerous studies have found a close relationship between hyperhomocysteinemia and oxidative stress, endoplasmic reticulum stress, endothelial cell injury as well as increased viscosity of blood, but the underlying mechanisms are largely unknown. This brief review introduces protein homocysteinylation, to which more and more researchers abroad begin to pay attention. We mainly focus on homocysteinylation of antioxidant enzymes, endoplasmic reticulum resident proteins, coagulation factors, low-density lipoprotein and calcium signaling-related proteins. To elucidate an importance of protein homocysteinylation in the development of atherosclerotic plaque, we also describe how homocysteine and its derivative homocysteine thiolactone covalently modify proteins, by which the structure and physical-chemical properties of target molecules are altered.

Key words: vascular endothelial cell, hyperhomocysteinemia, atherosclerosis, oxidative stress, endoplasmic reticulum stress

CLC Number:

R362
R543.5

WU Yun-Fei, ZHONG Liang-Wei. Protein homocysteinylation and mechanisms of atherosclerosis[J]. , 2009, 26(2): 145-151.

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