Hormonal
Metformin extends lifespan in C. elegans by inducing mitohormesis, a process where partial inhibition of mitochondrial complex I increases ROS production, which is translated into a longevity signal by the peroxiredoxin PRDX-2.
This research suggests that the longevity benefits of metformin in worms are driven by a specific stress-response pathway (mitohormesis) involving ROS and the protein PRDX-2. While this provides a mechanistic explanation for metformin's effects in a model organism, it does not directly translate to a human dosing protocol or guarantee similar lifespan extension in humans without further clinical validation.
We show that metformin extends lifespan through the process of mitohormesis and propose a signaling cascade in which metformin-induced production of reactive oxygen species increases overall life expectancy. We further address an important issue in aging research... We show that this beneficial signal of the mitohormetic pathway is propagated by the peroxiredoxin PRDX-2.
Why this rating
High-quality proteomics and genetic knockout data in a model organism, though translational to humans is not directly tested.
Source
Metformin promotes lifespan through mitohormesis via the peroxiredoxin PRDX-2
Wouter De Haes et al. · Proceedings of the National Academy of Sciences · 2014
DOI 10.1073/pnas.1321776111
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