Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2012 May 28:3:132.
doi: 10.3389/fphys.2012.00132. eCollection 2012.

Mechanisms involved in the aging-induced vascular dysfunction

Affiliations

Mechanisms involved in the aging-induced vascular dysfunction

Mariam El Assar et al. Front Physiol. .

Abstract

Vascular aging is a key process determining health status of aged population. Aging is an independent cardiovascular risk factor associated to an impairment of endothelial function, which is a very early and important event leading to cardiovascular disease. Vascular aging, formerly being considered an immutable and inexorable risk factor, is now viewed as a target process for intervention in order to achieve a healthier old age. A further knowledge of the mechanisms underlying the age-related vascular dysfunction is required to design an adequate therapeutic strategy to prevent or restore this impairment of vascular functionality. Among the proposed mechanisms that contribute to age-dependent endothelial dysfunction, this review is focused on the following aspects occurring into the vascular wall: (1) the reduction of nitric oxide (NO) bioavailability, caused by diminished NO synthesis and/or by augmented NO scavenging due to oxidative stress, leading to peroxynitrite formation (ONOO(-)); (2) the possible sources involved in the enhancement of oxidative stress; (3) the increased activity of vasoconstrictor factors; and (4) the development of a low-grade pro-inflammatory environment. Synergisms and interactions between all these pathways are also analyzed. Finally, a brief summary of some cellular mechanisms related to endothelial cell senescence (including telomere and telomerase, stress-induced senescence, as well as sirtuins) are implemented, as they are likely involved in the age-dependent endothelial dysfunction, as well as in the lower vascular repairing capacity observed in the elderly. Prevention or reversion of those mechanisms leading to endothelial dysfunction through life style modifications or pharmacological interventions could markedly improve cardiovascular health in older people.

Keywords: aging; cardiovascular disease; endothelial dysfunction; inflammation; nitric oxide; oxidative stress; senescence.

PubMed Disclaimer

Figures

Figure 1
Figure 1
Mechanisms involved in the aging-induced impairment of endothelial vasodilation.

References

    1. Abbatecola A. M., Paolisso G., Fattoretti P., Evans W. J., Fiore V., Dicioccio L., Lattanzio F. (2011). Discovering pathways of sarcopenia in older adults: a role for insulin resistance on mitochondria dysfunction. J. Nutr. Health Aging 15, 890–89510.1007/s12603-011-0366-0 - DOI - PubMed
    1. Ahlers B. A., Parnell M. M., Chin-Dusting J. P., Kaye D. M. (2004). An age-related decline in endothelial function is not associated with alterations in L-arginine transport in humans. J. Hypertens. 22, 321–32710.1097/00004872-200402000-00016 - DOI - PubMed
    1. Albarwani S., Al-Siyabi S., Baomar H., Hassan M. O. (2010). Exercise training attenuates ageing-induced BKCa channel downregulation in rat coronary arteries. Exp. Physiol. 95, 746–75510.1113/expphysiol.2009.051250 - DOI - PubMed
    1. Alcendor R. R., Gao S., Zhai P., Zablocki D., Holle E., Yu X., Tian B., Wagner T., Vatner S. F., Sadoshima J. (2007). Sirt1 regulates aging and resistance to oxidative stress in the heart. Circ. Res. 100, 1512–152110.1161/01.RES.0000267723.65696.4a - DOI - PubMed
    1. Angulo J., Cuevas P., Fernandez A., Gabancho S., Videla S., Saenz De Tejada I. (2003). Calcium dobesilate potentiates endothelium-derived hyperpolarizing factor-mediated relaxation of human penile resistance arteries. Br. J. Pharmacol. 139, 854–86210.1038/sj.bjp.0705293 - DOI - PMC - PubMed