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LDL biochemical modifications: a link between atherosclerosis and aging.

Matilde Alique1, Carlos Luna2, Julia Carracedo2

  • 1Departamento Biología de Sistemas, Facultad de Medicina y Ciencias de la Salud, Universidad de Alcalá, Madrid, Spain; matilde.alique@uah.es.

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Aging accelerates atherosclerosis by modifying low-density lipoprotein (LDL) and increasing reactive oxygen species (ROS). This leads to endothelial damage and cellular senescence, key markers of this age-related cardiovascular disease.

Keywords:
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Area of Science:

  • Cardiovascular Science
  • Aging Research
  • Biochemistry

Background:

  • Atherosclerosis is strongly linked to aging, with increasing age as a primary risk factor.
  • Modified low-density lipoprotein (LDL) is a significant risk marker for cardiovascular disease.
  • LDL modifications like oxidation, glycosylation, carbamylation, and glycoxidation are proatherogenic.

Purpose of the Study:

  • To review LDL modifications in the context of atherosclerosis.
  • To discuss the mechanisms linking aging, endothelial damage, oxidative stress, and atherosclerosis.
  • To explore the relationship between aging and the pathology of atherosclerosis.

Main Methods:

  • Review of existing literature on LDL modifications and atherosclerosis.
  • Analysis of experimental data (in vitro and in vivo) on proatherogenic effects of modified LDL.
  • Examination of the role of reactive oxygen species (ROS) and oxidative stress in endothelial damage and senescence.

Main Results:

  • High plasma LDL concentrations and specific modifications promote atherosclerosis.
  • Reactive oxygen species (ROS) in the arterial wall alter LDL, contributing to atherosclerosis.
  • Oxidative stress induces endothelial senescence, a well-established marker for atherosclerosis.

Conclusions:

  • Aging is a critical factor in atherosclerosis development.
  • Endothelial damage and cellular senescence, driven by oxidative stress and modified LDL, are key pathological mechanisms.
  • Understanding LDL modifications and oxidative stress is crucial for addressing age-related atherosclerosis.