» Articles » PMID: 20096766

Mitochondrial DNA Repair and Association with Aging--an Update

Overview
Journal Exp Gerontol
Specialty Geriatrics
Date 2010 Jan 26
PMID 20096766
Citations 70
Authors
Affiliations
Soon will be listed here.
Abstract

Mitochondrial DNA is constantly exposed to oxidative injury. Due to its location close to the main site of reactive oxygen species, the inner mitochondrial membrane, mtDNA is more susceptible than nuclear DNA to oxidative damage. The accumulation of DNA damage is thought to play a critical role in the aging process and to be particularly deleterious in post-mitotic cells. Thus, DNA repair is an important mechanism for maintenance of genomic integrity. Despite the importance of mitochondria in the aging process, it was thought for many years that mitochondria lacked an enzymatic DNA repair system comparable to that in the nuclear compartment. However, it is now well established that DNA repair actively takes place in mitochondria. Oxidative DNA damage processing, base excision repair mechanisms were the first to be described in these organelles, and consequently the best understood. However, new proteins and novel DNA repair pathways, thought to be exclusively present in the nucleus, have recently been described also to be present in mitochondria. Here we review the main mitochondrial DNA repair pathways and their association with the aging process.

Citing Articles

Characterization of dUTPase expression in mouse postnatal development and adult neurogenesis.

Nagy N, Hadinger N, Toth O, Racz G, Pinter T, Gal Z Sci Rep. 2024; 14(1):13139.

PMID: 38849394 PMC: 11161619. DOI: 10.1038/s41598-024-63405-0.


Mitochondrial DNA leakage triggers inflammation in age-related cardiovascular diseases.

Ding W, Chen J, Zhao L, Wu S, Chen X, Chen H Front Cell Dev Biol. 2024; 12:1287447.

PMID: 38425502 PMC: 10902119. DOI: 10.3389/fcell.2024.1287447.


First Report of Mitochondrial DNA Copy Number Variation in (Insecta, Hemiptera, Cicadellidae) from Polluted and Control Sites.

Calogero G, Giuga M, DUrso V, Ferrito V, Pappalardo A Animals (Basel). 2023; 13(11).

PMID: 37889727 PMC: 10251845. DOI: 10.3390/ani13111793.


Dysfunction of the neurovascular unit in brain aging.

Liu S, Yang X, Chen F, Cai Z J Biomed Res. 2023; 37(3):153-165.

PMID: 37198158 PMC: 10226086. DOI: 10.7555/JBR.36.20220105.


Endothelial Dysfunction in Neurodegenerative Diseases.

Fang Y, Hsieh Y, Hu C, Tu Y Int J Mol Sci. 2023; 24(3).

PMID: 36769234 PMC: 9918222. DOI: 10.3390/ijms24032909.


References
1.
Weissman L, de Souza-Pinto N, Stevnsner T, Bohr V . DNA repair, mitochondria, and neurodegeneration. Neuroscience. 2006; 145(4):1318-29. DOI: 10.1016/j.neuroscience.2006.08.061. View

2.
Hu J, de Souza-Pinto N, Haraguchi K, Hogue B, Jaruga P, Greenberg M . Repair of formamidopyrimidines in DNA involves different glycosylases: role of the OGG1, NTH1, and NEIL1 enzymes. J Biol Chem. 2005; 280(49):40544-51. DOI: 10.1074/jbc.M508772200. View

3.
de Souza-Pinto N, Wilson 3rd D, Stevnsner T, Bohr V . Mitochondrial DNA, base excision repair and neurodegeneration. DNA Repair (Amst). 2008; 7(7):1098-109. PMC: 4625841. DOI: 10.1016/j.dnarep.2008.03.011. View

4.
Liu P, Qian L, Sung J, de Souza-Pinto N, Zheng L, Bogenhagen D . Removal of oxidative DNA damage via FEN1-dependent long-patch base excision repair in human cell mitochondria. Mol Cell Biol. 2008; 28(16):4975-87. PMC: 2519700. DOI: 10.1128/MCB.00457-08. View

5.
Borghouts C, Kimpel E, Osiewacz H . Mitochondrial DNA rearrangements of Podospora anserina are under the control of the nuclear gene grisea. Proc Natl Acad Sci U S A. 1997; 94(20):10768-73. PMC: 23480. DOI: 10.1073/pnas.94.20.10768. View