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The mitochondrial genome in aging and senescence
Affiliation:1. Departamento de Fisiología, Facultad de Medicina, Centro de Investigación Biomédica, Parque Tecnológico de Ciencias de la Salud, Universidad de Granada, Granada, Spain;2. CIBERfes, Ibs.Granada, and UGC de Laboratorios Clínicos, Complejo Hospitalario de Granada, Granada, Spain;3. CIBERfes, División de Medicina Geriátrica, Hospital Virgen del Valle, Complejo Hospitalario de Toledo, Toledo, Spain;4. CIBERfes, Servicio de Geriatría, Hospital Universitario de Getafe, Madrid, Spain
Abstract:
Aging is characterized by a progressive decline in organism functions due to the impairment of all organs. The deterioration of both proliferative tissues in liver, skin and the vascular system, as well as of largely post-mitotic organs, such as the heart and brain could be attributed at least in part to cell senescence.In this review we examine the role of mitochondrial dysfunction and mtDNA mutations in cell aging and senescence. Specifically, we address how p53 and telomerase reverse transcriptase (TERT) activity switch their roles from cytoprotective to detrimental and also examine the role of microRNAs in cell aging. The proposed role of Reactive Oxygen Species (ROS), both as mutating agents and as signalling molecules, underlying these processes is also described.
Keywords:Aging  Senescence  Mitochondria  mtDNA  ROS  Molecular mechanisms
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