Many methods demonstrated to slow aging in short-lived species, such as the nematode worm Caenorhabditis elegans, involve hormesis. This is the induction of mild cellular stress and damage, through heat, or lack of nutrients, or raised levels of oxidative molecules generated by mitochondria, that leads to an enhanced cellular maintenance response. The net result is a gain in health and tissue function. The open access paper here discusses some of the known hormetic mechanisms in nematodes, those involving alterations in mitochondrial function, and illustrates one of many methods of triggering mitochondrial hormesis in that species. The degree to which longevity is enhanced in this case is not large at all when considering the plasticity of life span in nematodes; life spans in this species have been extended by a factor of ten by some research groups. Sadly, we know that these approaches have nowhere near the same outcome in mammals.
Alterations in microRNA (miRNA) processing have been previously linked to aging. Here we used the small molecule enoxacin to pharmacologically interfere with miRNA biogenesis and study how it affects aging in C. elegans. Enoxacin extended worm lifespan and promoted survival under normal and oxidative
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