Generic placeholder image

Current Pharmaceutical Design

Editor-in-Chief

ISSN (Print): 1381-6128
ISSN (Online): 1873-4286

Molecular Markers of Cardiovascular Damage in Hypertension

Author(s): Chiara Armani, Nicoletta Botto, Maria Grazia Andreassi and Emilio Centaro

Volume 19, Issue 13, 2013

Page: [2341 - 2350] Pages: 10

DOI: 10.2174/1381612811319130002

Price: $65

conference banner
Abstract

There is increasing evidence that an elevation of oxidative stress and associated oxidative damages are mediators of vascular injury in various cardiovascular pathologies, including hypertension. Accumulation of oxidative damage is thought to play an important role in aging and age-associated diseases such as hypertension and oxidative stress may function as a common trigger for activation of the senescence programme. In this regard, the role of telomeres in the onset, development and prognosis of hypertension has generated considerable interest. These structures may deteriorate in the onset and development of arterial hypertension in which their length may be a predictor of outcome. As telomere length by its nature is a marker of cell senescence, this parameter is of particular interest when studying the lifespan and fate of endothelial cells, cardiomyocytes and smooth muscle cells, especially so because telomere length seems to be regulated by various factors notably certain cardiovascular risk factors, such as smoking, sex and obesity that are associated with high levels of oxidative stress. This review focuses on the vascular effects of reactive oxygen species and the role of oxidative stress in hypertension- associated vascular damage. In addition it reviewes the considerable amount of data published recently on the role of telomeres to gain insights into the links between telomere length and hypertension, and assesses the usefulness of telomere length as a new marker of cardiovascular risk.

Keywords: Telomere, telomerase, hypertension, oxidative stress, oxidative damages, vascular injury, marker, cell senescence, endothelial cells, cardiomyocytes


Rights & Permissions Print Cite
© 2024 Bentham Science Publishers | Privacy Policy