The mitochondrial genome in aging and senescence

Ageing Res Rev. 2014 Nov:18:1-15. doi: 10.1016/j.arr.2014.07.001. Epub 2014 Jul 17.

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; Mitochondria; Molecular mechanisms; ROS; Senescence; mtDNA.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Aging / genetics*
  • Aging / metabolism
  • Aging / pathology
  • Animals
  • Autophagy / genetics
  • Cellular Senescence / genetics*
  • DNA, Mitochondrial / genetics*
  • DNA, Mitochondrial / metabolism
  • Genome, Human*
  • Humans
  • Mitochondria / metabolism*
  • Mitochondria / pathology
  • Mutation
  • Reactive Oxygen Species
  • Signal Transduction
  • Telomerase / metabolism
  • Tumor Suppressor Protein p53 / metabolism

Substances

  • DNA, Mitochondrial
  • Reactive Oxygen Species
  • TP53 protein, human
  • Tumor Suppressor Protein p53
  • TERT protein, human
  • Telomerase