IMR Press / FBL / Volume 13 / Issue 13 / DOI: 10.2741/3064

Frontiers in Bioscience-Landmark (FBL) is published by IMR Press from Volume 26 Issue 5 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on imrpress.com as a courtesy and upon agreement with Frontiers in Bioscience.

Article
Oxidative stress in vascular senescence: lessons from successfully aging species
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1 Department of Physiology, New York Medical College, Valhalla, New York 10595, USA
2 The Sam and Ann Barshop Institute for Longevity and Aging Studies, The University of Texas Health Science Center, San Antonio, Texas 78245

*Author to whom correspondence should be addressed.

 

Front. Biosci. (Landmark Ed) 2008, 13(13), 5056–5070; https://doi.org/10.2741/3064
Published: 1 May 2008
Abstract

Cardiovascular disease is a main cause of morbidity and a leading cause of death of elderly Americans. Studies identifying the pathophysiological mechanisms underlying cardiovascular aging hold promise to develop treatments to delay/prevent coronary artery disease and stroke in the elderly. Evidence supporting the roles of oxidative stress and inflammation in the cardiovascular aging process is presented in detail in this review. Mammalian lifespan ranges hundred-fold and we propose that long-living species may be useful models for successful cardiovascular aging in humans. Comparative studies exploiting the large differences in maximum lifespan potential and cardiovascular aging patterns may be particularly relevant. Comparisons of mechanisms related to oxidative stress, oxidative stress resistance and redox signaling between long-living species and shorter-living ones may elucidate key mechanisms for delaying cardiovascular aging. We discuss the potential use of three long-lived but mouse-sized mammalian species, the naked mole-rat (Heterocephalus glaber), the white-footed mouse (Peromyscus leucopus) and the little brown bat (Myotis lucifugus) to test predictions of the oxidative stress theory of aging and elucidate mechanisms by which cardiovascular aging can be delayed.

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