**3. Conclusions**

Aging is a consequence of damage accumulation in different cellular constituents and where DNA damage is one of the most important. Every day there are thousands of insults that affect DNA, either due to endogenous factors (such as metabolism) or exogenous factor like contact with radiation sources or exposure to toxic substances; but only a minimal amount (less than 0.02%) accumulates as permanent damage, while the rest is totally repaired. However, if only one gene is not repaired and its function is important as that of a proto-oncogene, a tumor suppressor, or any DNA repair genes, this could lead to accumulation of mutations, and then DNA damage checkpoints can halt the cell cycle and induce cellular senescence or apoptosis, or well erroneous repair or replicative bypass of lesions can result in mutations and chromosomal aberrations leading the cells to transform into cancer cells.

Notably, DNA repair systems are able of dealing with most of the damages inflicted to DNA; however, their efficiency decrease with age, permitting that point mutations, insertions, deletions, and rearrangements, among others, occur more frequently and accumulate over time. This is due in part to the fact that critical proteins involved in DNA repair significantly decrease their expression in an agerelated manner. In **Figure 2**, the main age-related changes reported over the different mechanisms of DNA repair together with their consequences that globally cause genomic instability and favor cellular senescence and cancer are summarized.

 Overall, this area needs to be more exploited in order to improve our quality of life and prevent or delay the harmful effects of aging. Thus, the more knowledge we acquire about the natural cell aging process and its interrelation with the mechanisms of DNA repair, the closer we will be to develop drugs, therapies, or even vaccines that could help us to prolong our life.
