Oxidative Stress in Aging-Matters of the Heart and Mind

被引:108
作者
Venkataraman, Krishnan [1 ]
Khurana, Sandhya [2 ]
Tai, T. C. [2 ,3 ]
机构
[1] Huntington Univ, Dept Gerontol, Sudbury, ON P3E 2C6, Canada
[2] Northern Ontario Sch Med, Div Med Sci, Sudbury, ON P3E 2C6, Canada
[3] Laurentian Univ, Dept Biol, Dept Chem & Biochem, Biomol Sci Program, Sudbury, ON P3E 2C6, Canada
关键词
oxidative stress; RONS; cardiovascular; aging; brain; ADHESION MOLECULE-1 VCAM-1; NF-KAPPA-B; PLASMINOGEN-ACTIVATOR INHIBITOR-1; ADVANCED GLYCATION ENDPRODUCTS; RENIN-ANGIOTENSIN SYSTEM; TUMOR-NECROSIS-FACTOR; CALORIC RESTRICTION; ALZHEIMERS-DISEASE; L-ARGININE; ENDOTHELIAL DYSFUNCTION;
D O I
10.3390/ijms140917897
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Oxidative damage is considered to be the primary cause of several aging associated disease pathologies. Cumulative oxidative damage tends to be pervasive among cellular macromolecules, impacting proteins, lipids, RNA and DNA of cells. At a systemic level, events subsequent to oxidative damage induce an inflammatory response to sites of oxidative damage, often contributing to additional oxidative stress. At a cellular level, oxidative damage to mitochondria results in acidification of the cytoplasm and release of cytochrome c, causing apoptosis. This review summarizes findings in the literature on oxidative stress and consequent damage on cells and tissues of the cardiovascular system and the central nervous system, with a focus on aging-related diseases that have well-documented evidence of oxidative damage in initiation and/or progression of the disease. The current understanding of the cellular mechanisms with a focus on macromolecular damage, impacted cellular pathways and gross morphological changes associated with oxidative damage is also reviewed. Additionally, the impact of calorific restriction with its profound impact on cardiovascular and neuronal aging is addressed.
引用
收藏
页码:17897 / 17925
页数:29
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