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‘To repair or not to repair – no longer a question’: repair of mitochondrial DNA shielding against age and cancer
Author(s) -
Berneburg Mark,
Kamenisch York,
Krutmann Jean,
Röcken Martin
Publication year - 2006
Publication title -
experimental dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.108
H-Index - 96
eISSN - 1600-0625
pISSN - 0906-6705
DOI - 10.1111/j.1600-0625.2006.00508.x
Subject(s) - mitochondrial dna , mitochondrion , dna repair , base excision repair , nucleotide excision repair , biology , carcinogenesis , dna damage , genetics , microbiology and biotechnology , cancer , dna , gene
The role of mitochondria in energy production and apoptosis is well known. The role of mitochondria and particularly the role of the mitochondria's own genome, mitochondrial (mt) DNA, in the process of ageing were postulated decades ago. However, this was discussed, debated and more or less disposed of. Recent data from elegant mouse models now confirm that mutations of mtDNA do indeed play a central and pivotal role in the ageing process. Newer reports also indicate a possible role of mtDNA mutations in the carcinogenesis of several organs. But is damaged mtDNA repaired, or is it simply degraded and discarded? This question appears to be answered now. According to recent data, mitochondria possess functional repair mechanisms such as base excision repair, double‐strand break repair and mismatch repair, yet nucleotide excision repair has so far not been detected.