Aging and Protein Kinases

Adv Exp Med Biol. 2021;1275:35-69. doi: 10.1007/978-3-030-49844-3_2.

Abstract

Recently, aging has been tried to be explained with large numbers of theories, but none of them can elucidate the changes occurring in the aging process alone. A unified theory encompassing the mechanisms of genetic factors and repair systems in aging is becoming increasingly required. Almost 37 protein kinases contribute to all processes of aging and senescence. Furthermore, these kinases not only regulate the large number of metabolic pathways related to aging processes, but also control these pathways through 12 checkpoints. Thus, in this chapter, the metabolic targets of protein kinases signal transduction pathways were discussed in terms of the aging perspective under five headings, which are the indispensable stages of the aging process. Although the most popular classical aging theories have been stated as DNA damage theory, mitochondrial theory, free radical theory, and telomere theory, it was concluded that the aging process is controlled by protein kinases regardless of the different theories.

Keywords: Ataxia- and Rad3-related (ATR); Ataxia-telangiectasia mutated (ATM); Base excision repair (BER); DNA damage; DNA damage response (DDR); DNA-dependent protein kinase, catalytic subunit (DNA-PKcs); Insulin-like growth factor signaling (IIS); Mammalian target of rapamycin complex 1 (mTORC1); Nucleotide excision repair (NER); Polo-like kinase-1 (PLK1).

MeSH terms

  • Ataxia Telangiectasia Mutated Proteins / genetics
  • Cell Cycle Proteins / metabolism
  • DNA Damage*
  • DNA Repair
  • Protein Kinases* / genetics
  • Signal Transduction

Substances

  • Cell Cycle Proteins
  • Protein Kinases
  • Ataxia Telangiectasia Mutated Proteins