During the last 20 years, the Mitochondrial Theory of Ageing (MTA) has been one of the most supported theories to explain ageing. Different animal models (Saccharomyces cerevisiae, Caenorhabditis elegans, Drosophila melanogaster, and Mus musculus) support the hypothesis that mitochondria play an essential role in ageing process; however there is a lot of controversy about the mechanism by how they influence on longevity. Several explanations (some time contradictory, some time complementary) have been proposed. The most supported are based on free radical chemistry, alterations of redox homeostasis, deficits in ATP production, deregulation of apoptosis, and the accumulation of mutations in the mitochondrial DNA. The understanding of ageing phenomenon requires determining the role mitochondria play on it, discerning if the alteration in mitochondrial function associated to ageing is a cause or a consequence of it.

We invite researchers to contribute with original research articles as well as review articles that will help to understand the biochemical, molecular, and physiological mechanisms behind ageing, as well as new strategies to delay or even reverse the ageing process increasing the numbers of healthy years. We are particularly interested in articles dealing with the role mitochondria play in ageing (passive or active), and particularly in the accumulation of mutations in mitochondrial DNA, the regulation of mitochondrial free radical production, and the discovery of new signaling pathways in the crosstalk between nuclei and mitochondria. In addition, articles focusing in new techniques to measure mutations rate in mitochondrial DNA and generation of oxidative damage (including ROS production) in vivo would be greatly appreciated.

Potential topics include, but not limited to:

• Ageing and evolution
• Oxidative stress markers of ageing
• Crosstalking between the nucleus and mitochondria
• Cancer and mitochondria
• New techniques for the measurement of free radical generation in vivo
• New techniques to evaluate the accumulation of mutations in mtDNA
• Therapies to delay aging
• Therapies to reverse aging

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