The mitochondrial genome in aging and senescence

• Mitochondria are central to aging.
• mtDNA mutations can cause aging.
• ROS are central in aging and senescence as mutating agent and signaling molecules.
• ROS induce p53 and TERT switch from protective to detrimental activity.
• miRNAs contribute to aging and senescence by targeting mitochondrial processes.

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.

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