Mitochondria are the power plants of the cell, generating the chemical energy store molecule adenosine triphosphate (ATP). Throughout the body, mitochondrial function declines with age, leading to corresponding declines in tissue and organ function. This universal malaise appears to be a downstream consequence of the underlying causes of aging. Those causes in some way lead to changes in gene expression that alter mitochondrial dynamics in ways that reduce the efficacy of the quality control mechanism of mitophagy. When not regularly destroyed, worn and dysfunctional mitochondria accumulate, and ATP production suffers.
It is possible to achieve benefits by introducing replacement mitochondria? Won’t they just succumb to the same problem due to the aged environment? Eventually, yes, most likely. But studies to date suggest that the benefits of mitochondrial transplantation can large enough and long-lasting enough to be worth pursuing, even if the benefits fade over time.
Cells will readily take up whole mitochondria from their environment, and thus the immediate hurdles are largely a matter of logistics: being able to reliably generate and characterize mitochondria in the vast numbers needed to make a difference
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