RNA Interference of ATP Synthase Subunits Slows Aging in Nematodes

Mitochondria are the power plants of the cell, responsible for generating adenosine triphosphate (ATP), a chemical energy store molecule used to power cellular operations. The inner workings of each mitochondrion are energetic and complicated, consisting of a number of interacting protein complexes that collectively perform the work needed to manufacture ATP molecules. Mitochondrial function occupies a central position in the interaction between metabolism and aging for a number of reasons. Firstly, they generate reactive oxygen species (ROS) as a side effect of ATP production, and the flux of ROS is both damaging and a signal to the cell to step up its efforts to repair damage. A little more ROS than usual can be beneficial. Too much ROS is harmful. Secondly, some of the critical proteins in mitochondrial complexes are produced from DNA inside the mitochondria rather than in the cell nucleus, and that DNA is vulnerable to damage. Some forms of mitochondrial DNA damage can produce damaged mitochondria that cause great harm to the cell and surrounding tissue. Thirdly, cells need ATP, and reductions in ATP production have detrimental consequences over time. There are many ways in which mitochondrial function can be altered through the removal or reduced production of a specific subunit of one of the mitochondrial protein complexes. Some such changes are disastrous, some are beneficial. Why that is the case is a complicated topic. It has a great deal to do with the balanc...
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