Send to

Choose Destination
Biogerontology. 2018 Jul;19(3-4):189-208. doi: 10.1007/s10522-018-9748-6. Epub 2018 Feb 28.

Mitochondria, its DNA and telomeres in ageing and human population.

Zole E1,2, Ranka R3,4.

Author information

Latvian Biomedical Research and Study Centre, Ratsupites Street 1, Riga, 1067, Latvia.
Faculty of Biology, University of Latvia, Jelgavas Street 1, Riga, 1004, Latvia.
Latvian Biomedical Research and Study Centre, Ratsupites Street 1, Riga, 1067, Latvia.
Riga Stradins University, Dzirciema iela 16, Riga, 1007, Latvia.


In the last decades, studies about ageing have become more essential as our population grows older. The incidence of age-related diseases increases, which pose challenges both for societies and individuals in terms of life quality and economic impact. Understanding ageing and ageing-related processes will help us to slow down or even prevent these diseases and provide opportunities for healthy ageing; additionally, we all want to live longer. Ageing is a consequence of the interaction between processes that occur over time and genetics interacting with various disease states and an individual's lifestyle. There are several hallmarks of ageing that are generally accepted, but neither of the theories appears to be fully satisfactory. The focus of this article is on two theories of ageing: telomere shortening and mitochondrial DNA (mtDNA) alterations and dysfunction. We discuss characteristic molecular features such as mitochondrial haplogroups, telomere length, mtDNA copy number and heteroplasmy, and how all these traits come together in the ageing population. The recent evidence shows the existence of a strong linkage between these two theories suggesting common molecular mechanisms and a complicated telomere-mitochondria interplay during the humans' ageing. However, this relationship is still not completely understood, which is why it needs more attention.


Heteroplasmy; Mitochondrial haplogroups; Population ageing; Telomere length; mtDNA copy number

[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Springer
Loading ...
Support Center