Research in Mitochondrial Signals and Extended Lifespan

This is interesting research: scientists "used the roundworm Ceanorhabditis elegans to show that perturbing mitochondrial function in subsets of worm cells sent global signals governing longevity of the entire organism. ... In this study we show how signals sent from distressed mitochondria are communicated to distant tissues to promote survival and enhance longevity ... The identity of the signal sent from mitochondrially-distressed cells - a hypothetical factor Dillin calls a 'mitokine' - remains unknown. Nonetheless, he speculates that mitokines could one day be lobbed as messengers from healthy to unhealthy tissues to treat degenerative conditions. ... Imagine if we could perturb mitochondria in the liver, and make them send a mitokine to degenerating neurons. Instead of trying to get a drug into the brain, we could exploit the body's ability to send out a natural rescue signal. ... many investigators, Dillin included, have observed puzzling relationships between mitochondria, energy generation and longevity-interactions that suggest that living long does not necessarily require prospering at the subcellular level. ... As a postdoctoral fellow I did a screen looking for worm genes that increased longevity. Many genes were related to mitochondrial function. If you disabled them, worms lived longer, although their respiration or metabolism was reduced. We wondered whether this is why animals lived longer. ... To determine how cells respond to the pro-longevity cue, the group monitored a cellular emergency plan called the Unfolded Protein Response (UPR). Cells mount it when proteins accumulate excessively and begin to unravel - or 'misfold' - which is toxic to cells. To avert cell death, the UPR mobilizes a team of helpers who, like sales clerks at a Gap sweater table, refold accumulating misfolded proteins piling up inside a cell. When Dillin and colleagues fed worms reagents blocking the UPR, they found that disruption of [mitochondrial activity] in neurons or intestine no longer had a lifespan-enhancing effect. This dramatic finding illustrates that initiating refolding of proteins, in this case in response to faraway mitochondrial stress, is in fact the very activity that enhances longevity." You might compare this to the benefits of autophagy, another housekeeping and repair activity that takes place inside cells.



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