Sammanfattning
therosclerosis 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.