Answers are grounded in this paper and cite their sources.
Atherosclerosis is an aging disease in which increasing age is a risk factor. Modified low-density lipoprotein (LDL) is a well-known risk marker for cardiovascular disease. High-plasma LDL concentrations and modifications, such as oxidation, glycosylation, carbamylation and glycoxidation, have been shown to be proatherogenic experimentally in vitro and in vivo. Atherosclerosis results from alterations to LDL in the arterial wall by reactive oxygen species (ROS). Evidence suggests that common risk factors for atherosclerosis raise the likelihood that free ROS are produced from endothelial cells and other cells. Furthermore, oxidative stress is an important factor in the induction of endothelial senescence. Thus, endothelial damage and cellular senescence are well-established markers for atherosclerosis. This review examines LDL modifications and discusses the mechanisms of the pathology of atherosclerosis due to aging, including endothelial damage and oxidative stress, and the link between aging and atherosclerosis.Keywords: aging; atherosclerosis; endothelial damage; LDL modifications; oxidative stress(Published: 3 December 2015)Citation: Food & Nutrition Research 2015, 59: 29240 - http://dx.doi.org/10.3402/fnr.v59.29240
No takes yet. Share an insight, caveat, or question.
Alique et al. (2015) studied this question.
Synapse has enriched 10 related papers. Consider them for comparative context: