DNA repair mechanisms are crucial for maintaining genomic stability, and their efficiency declines with age, leading to increased DNA damage in cells such as leukocytes, sperm, and oocytes.

Research shows that long-lived populations tend to have enhanced DNA repair systems, highlighting a strong link between effective DNA repair and longevity.

Genomic instability, a hallmark of aging, underscores the importance of understanding DNA repair pathways to develop interventions against age-related diseases.

Multiple DNA repair pathways, including homologous recombination, nonhomologous end joining, base excision repair, and nucleotide excision repair, are vital for fixing DNA damage.

DNA damage occurs frequently due to various sources, making efficient repair systems essential for cellular and organ health.

As humans age, the decline in DNA repair efficiency contributes to the accumulation of DNA damage, which is a key factor in aging.

Further research is needed to understand the tissue-specific, sex-dependent, and population-related variability in DNA repair regulation as it relates to aging.

Mutations in certain genes linked to DNA repair deficiencies are associated with accelerated aging syndromes such as Werner, Cockayne, and Hutchinson-Gilford Progeria.

Future studies should focus on translating mechanistic insights of DNA repair into clinical applications to improve health and extend lifespan.