The open access paper here presents an interesting result in mitochondrial biology. Mitochondria are the power plants of the cell, a herd of bacteria-like structures responsible for packaging chemical energy store molecules. They have their own small genome of a few mitochondrial genes. A mitochondrion may have one or several copies of this genome, and mitochondria promiscuously fuse together, divide, and swap around their component parts from one to another. This makes it quite hard to understand how their age-related dysfunction and damage progresses in detail.
Nonetheless, it is well demonstrated that mitochondria become progressively less functional with advancing age, and this is particularly relevant in energy-hungry tissues such as muscles and the brain. Some of this decline may be reaction to forms of cell and tissue damage, and some of this is due to stochastic mutational damage occurring to mitochondrial DNA. In this context, the researchers here show that forcing an increase in the number of copies of mitochondrial DNA can maintain mitochondrial function in old age, and thereby slow vascular aging. It remains unclear, however, as to the exact chain of mechanisms that make this the case: the causes and immediate consequences of an age-related
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