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Aging and Disease    2014, Vol. 5 Issue (2) : 101-108     DOI: 10.14336/AD.2014.0500101
Aging and Injury: Alterations in Cellular Energetics and Organ Function
Ninu Poulose1, Raghavan Raju1, 2, *
1Department of Medical Laboratory, Imaging and Radiological Sciences, Georgia Regents University, Augusta, GA30912, USA
2Biochemistry and Molecular Biology, Georgia Regents University, Augusta, GA30912, USA
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Aging is characterized by increased oxidative stress, heightened inflammatory response, accelerated cellular senescence and progressive organ dysfunction. The homeostatic imbalance with aging significantly alters cellular responses to injury. Though it is unclear whether cellular energetic imbalance is a cause or effect of the aging process, preservation of mitochondrial function has been reported to be important in organ function restoration following severe injury. Unintentional injuries are ranked among the top 10 causes of death in adults of both sexes, 65 years and older. Aging associated decline in mitochondrial function has been shown to enhance the vulnerability of heart, lung, liver and kidney to ischemia/reperfusion injury. Studies have identified alterations in the level or activity of factors such as SIRT1, PGC-1α, HIF-1α and c-MYC involved in key regulatory processes in the maintenance of mitochondrial structural integrity, biogenesis and function. Studies using experimental models of hemorrhagic injury and burn have demonstrated significant influence of aging in metabolic regulation and organ function. Understanding the age-associated molecular mechanisms regulating mitochondrial dysfunction following injury is important towards identifying novel targets and therapeutic strategies to improve the outcome after injury in the elderly.

Keywords aging      hemorrhage      ischemia      mitochondria      sirt1      hypoxia     
Corresponding Authors: Raghavan Raju   
Issue Date: 10 March 2014
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Ninu Poulose,Raghavan Raju. Aging and Injury: Alterations in Cellular Energetics and Organ Function[J]. Aging and Disease, 2014, 5(2): 101-108.
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