Browse by author
Lookup NU author(s): Dr Joao Passos,
Professor Thomas von Zglinicki,
Emeritus Professor Thomas Kirkwood
Full text for this publication is not currently held within this repository. Alternative links are provided below where available.
Mitochondrial dysfunction has long been considered a key mechanism in the ageing process but surprisingly little attention has been paid to the impact of mitochondrial number or density within cells. Recent reports suggest a positive association between mitochondrial density, energy homeostasis and longevity. However, mitochondrial number also determines the number of sites generating reactive oxygen species (ROS) and we suggest that the links between mitochondrial density and ageing are more complex, potentially acting in both directions. The idea that increased density, especially when combined with mitochondrial dysfunction, might accelerate ageing is supported by a negative correlation between mitochondrial density and maximum longevity in an interspecies comparison in mammals, and by evidence for an intimate interconnection between cellular ROS levels, mitochondrial density and cellular ageing. Recent data suggest that retrograde response, which activates mitochondrial biogenesis, accompanies cellular ageing processes. We hypothesise that increased mitochondrial biogenesis, and possibly also impaired degradation and segregation of mitochondria, if occurring as adaptation to pre-existing mitochondrial dysfunction, might aggravate ROS production and thus actively contribute to ageing. © 2007 Wiley Periodicals, Inc.
Author(s): Passos JF, Von Zglinicki T, Kirkwood TBL
Publication type: Article
Publication status: Published
Print publication date: 01/09/2007
ISSN (print): 0265-9247
ISSN (electronic): 1521-1878
PubMed id: 17688237
Altmetrics provided by Altmetric