Vascular aging is associated with structural and functional modifications of the arteries, and by an increase in arterial wall thickening in the intima and the media, mainly resulting from structural modifications of the extracellular matrix (ECM) components. Among the factors known to accumulate with aging, advanced lipid peroxidation end products (ALEs) are a hallmark of oxidative stress-associated diseases such as atherosclerosis. Aldehydes generated from the peroxidation of polyunsaturated fatty acids (PUFA), (4-hydroxynonenal, malondialdehyde, acrolein), form adducts on cellular proteins, leading to a progressive protein dysfunction with consequences in the pathophysiology of vascular aging. The contribution of these aldehydes to ECM modification is not known. 
This study was carried out to investigate whether aldehyde-adducts are 
detected in the intima and media in human aorta, whether their level is increased 
in vascular aging, and whether elastin fibers are a target of aldehyde-adduct 
formation
. 
Immunohistological and confocal immunofluorescence studies indicate 
that 4-HNE-histidine-adducts accumulate in an age-related manner in the intima, 
media and adventitia layers of human aortas, and are mainly expressed in smooth 
muscle cells. In contrast, even if the structure of elastin fiber is strongly 
altered in the aged vessels, our results show that elastin is not or very poorly

modified by 4-HNE
. These data indicate a complex role for lipid peroxidation and in particular for 4-HNE in elastin homeostasis, in the vascular wall remodeling during aging and atherosclerosis development.