There is a constantly replicating herd of mitochondria in every cell, the evolved descendants of ancient symbiotic bacteria now well integrated into cellular mechanisms. They still bear a small remnant of the original bacterial DNA, however, and this is prone to mutational damage. Some forms of this damage cause mitochondria to both malfunction and become more resilient or more able to replicate than their peers. As a result, the cell is quickly overtaken by broken mitochondria and becomes broken itself, exporting damaging reactive molecules into surrounding tissues, the bloodstream, and the body at large.
This process is one of the root causes of aging, so it is a matter of considerable interest to the research community to understand exactly how it is that these damaged mitochondria can so quickly replicate to fill a cell with their descendants. That said, the beauty of the SENS rejuvenation research approach to the problem is that it really doesn’t depend on how the damage occurs or spreads. It aims to place backup copies of mitochondrial genes into the cell nucleus, thus ensuring that there is always a supply of the proteins encoded in mitochondrial DNA. So if mitochondrial DNA does become
Article originally posted at