Proposing Synthetic Mitochondria as a Treatment for Aging
Mitochondria are the power plants of the cell, generating chemical energy stores used in many cellular processes. A herd of them exists in every cell, dividing like bacteria to keep up their numbers. Mitochondrial damage occurs as a side-effect of the normal operation of metabolism and is an important contribution to degenerative aging, but fortunately there are a wide range of fairly well understood methods by which this issue could be prevented or treated. All that is needed is more funding for research and development.
One possibility is the delivery of replacement mitochondria, and if doing this why not deliver better, more effective mitochondria? Some of the existing mitochondrial haplogroups are objectively better than others, but we could also in theory greatly improve upon what exists based on present knowledge. At the end of this road lies the replacement of mitochondria with optimal synthetic versions, resistant to damage, which influence surrounding cellular mechanisms in beneficial ways, and which minimize the mitochondrial contribution to aging. That isn't a near term prospect, but in the decades ahead it will become very plausible to start replacing more discrete cellular components with designed molecular machinery that is more efficient and less vulnerable, and thus helps to extend healthy life span:
We hypothesize herein that synthetic mitochondria, engineered or reprogrammed to be more energetically efficient and to have mildly elevated levels of reactive oxygen species (ROS) production, would be an effective form of therapeutics against systemic aging. The free radical and mitochondria theories of aging hold that mitochondria-generated ROS underlies chronic organelle, cell and tissues damages that contribute to systemic aging. More recent findings, however, collectively suggest that while acute and massive ROS generation during events such as tissue injury is indeed detrimental, subacute stresses and chronic elevation in ROS production may instead induce a state of mitochondrial hormesis (or "mitohormesis") that could extend lifespan.Mitohormesis appears to be a convergent mechanism for several known anti-aging signaling pathways. Importantly, mitohormetic signaling could also occur in a non-cell autonomous manner, with its induction in neurons affecting gut cells, for example. Technologies are outlined that could lead towards testing of the hypothesis, which include genetic and epigenetic engineering of the mitochondria, as well as intercellular transfer of mitochondria from transplanted helper cells to target tissues.