Mitochondria are the power plants of the cell, the descendants of ancient symbiotic bacteria. They retain a tiny remnant of the original bacterial genome, encoding thirteen genes essential to mitochondrial function. Most of the other genes moved to the cell nucleus over the course of evolutionary time, as mitochondria became ever more integrated as cellular components. Unfortunately mitochondrial DNA is more vulnerable to damage than nuclear DNA, and some forms of damage can produce malfunctioning mitochondria, faulty because they lack the essential proteins produced by now broken genes. These errant mitochondria can quickly overtake a cell, crowding out their undamaged peers. That cell then becomes a dysfunctional exporter of harmful oxidative molecules, an outcome that contributes to a range of age-related conditions. Oxidized lipids, for example, contribute to the progression of atherosclerosis.
The goal of the MitoSENS research program is to generate backup copies of all mitochondrial genes in the cell nucleus via gene therapy, a process known as allotopic expression. This will in principle prevent damage to mitochondrial DNA from contributing to aging, by providing an additional source of the proteins necessary for correct mitochondrial function. Of course, this is easier said than done, always true in