DNA repair is a collection of molecular pathways that detect and correct damage to the genetic material. Because DNA is constantly challenged by radiation, chemicals, reactive oxygen species and replication errors, cells rely on multiple complementary systems to maintain genome stability and prevent mutations that can lead to cancer, aging phenotypes and hereditary diseases.

Base excision repair fixes small, non‑distorting lesions such as oxidized or alkylated bases. Specialized DNA glycosylases recognize and remove damaged bases, creating abasic sites that are processed by endonucleases, polymerases and ligases to restore the correct sequence. Nucleotide excision repair removes bulky lesions like those caused by ultraviolet light. In this pathway, damage distorting the double helix is recognized, a short single‑stranded DNA segment containing the lesion is cut out and the gap is filled using the undamaged strand as a template.

Mismatch repair corrects replication errors that escape proofreading, such as mispaired bases and small insertions or deletions. It distinguishes the newly synthesized strand from the template, excises the error‑containing region and resynthesizes it accurately. Double‑strand breaks, among the most dangerous lesions, are repaired by nonhomologous end joining or homologous recombination. Nonhomologous end joining rapidly rejoins broken ends, often with small insertions or deletions, while homologous recombination uses a sister chromatid as a template to restore the original sequence with high fidelity.

Defects in these pathways are linked to cancer predisposition syndromes, neurodegeneration and premature aging. Understanding the molecular details of DNA repair has led to targeted therapies such as inhibitors that exploit specific repair weaknesses in tumor cells, and continues to guide research into genome maintenance and human disease.