title: LDL biochemical modifications: a link between atherosclerosis and aging.
abstract: 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.
authors.affiliation: Departamento Biología de Sistemas, Facultad de Medicina y Ciencias de la Salud, Universidad de Alcalá, Madrid, Spain; matilde.alique@uah.es.
authors.forename: Matilde
authors.initials: M
authors.lastname: Alique
authors.affiliation: Instituto Maimónides de Investigación Biomédica de Córdoba (IMIBIC), Hospital Universitario Reina Sofía, Universidad de Córdoba, Córdoba, Spain.
authors.forename: Carlos
authors.initials: C
authors.lastname: Luna
authors.affiliation: Instituto Maimónides de Investigación Biomédica de Córdoba (IMIBIC), Hospital Universitario Reina Sofía, Universidad de Córdoba, Córdoba, Spain.
authors.forename: Julia
authors.initials: J
authors.lastname: Carracedo
authors.affiliation: Departamento Biología de Sistemas, Facultad de Medicina y Ciencias de la Salud, Universidad de Alcalá, Madrid, Spain.
authors.forename: Rafael
authors.initials: R
authors.lastname: Ramírez
keywords: LDL modifications; aging; atherosclerosis; endothelial damage; oxidative stress