Arterial aging: a brief review

Vol. 53 No. 3 Suppl., 2012
This supplement was not sponsored by Outside Organizations.


Oana Mirea, I. Donoiu, I. E. Plesea

Aging is associated with changes in arterial wall structure and function that exceed physiological adaptation, with an increased risk of cardiovascular events. The most consistent structural changes are luminal enlargement (dilatation), wall thickening (remodeling), and a reduction of elastic properties. Endothelial dysfunction plays an important role in the functional changes that occur with age. New target therapies to prevent or reverse this process are under evaluation.

Corresponding author: Ionut Donoiu, MD; e-mail:

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Ana Marina Fusaru, Camelia Elena Stanciulescu, V. Surlin, C. Taisescu, Adriana Bold, O. T. Pop, Ileana Monica Banita, Stefania Craitoiu, Catalina Gabriela Pisoschi

White adipose tissue from different locations is characterized by significant differences in the structure of adipocyte "secretoma". Fat accumulation in the central-visceral depots is usually associated with a chronic inflammatory state, which is complicated by the metabolic syndrome. Recently, the adipose tissue was emerged to have an essential role in the innate immunity, adipocytes being considered effector cells due to the presence of the Toll-like receptors (TLRs). In this study, we compared the expression of TNF-alpha, TLR2 and TLR4 in peripheral-subcutaneous and central-peritoneal adipose depots in three different conditions - lean, obese and obese diabetic - using immunohistochemistry. Our results suggest a correlation between the incidence of the stromal vascular cells and adipocytes TNF-alpha and TLR4 in the visceral depots in strong correlation with adipose tissue expansion. TLR2 positive cells were seen in the peripheral depots from all groups without any association with fat accumulation. These results focus on the existence of a new pathogenic pathway, the activation of TLR4, for the involvement of visceral adipose tissue in the activation and maintenance of the inflammatory cascade in obesity.

Corresponding author: Catalina Gabriela Pisoschi, Professor, PhD; e-mail:

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