The open access paper I’ll point out today ties together a number of common themes in aging research. The authors propose that mitochondrial production of reactive oxygen species (ROS) is a significant cause of stochastic nuclear DNA damage, which in turn is a significant cause of cellular senescence. Those issues can then also disrupt mitochondrial function to increase ROS production, forming a feedback loop. In this view of the driving processes of aging, mitochondria are largely at fault for anything that can be pinned to rising levels of random mutations in nuclear DNA: cancer risk, cellular senescence, generally increased levels of cellular malfunction, and so forth.
An important caution regarding this paper is that the researchers used mice with a DNA repair deficiency in order to assemble their data. Such animals exhibit the appearance of accelerated aging, but it isn’t in fact accelerated aging. It is usually an excess of cellular damage that isn’t all that relevant in normal aging – any sort of global dysfunction in cells will tend to share high level similarities with aging, even if the damage is different. When it is significantly
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