MitoSENS to address mitochondrial diseases and aging


Mitochondria act as the “power plants” of cells, converting the energy-rich nutrients in our food into ATP, a form of energy that powers all cellular activity and function. While they are part of our cells, mitochondria have their own DNA (mtDNA). This DNA is separate from the DNA in our cells’ nuclei, which is much better protected from damage.

Mitochondria produce toxic waste products as part of the process of creating ATP energy. In this case, they send out free radicals that can damage the components of the cell when they strike them. The mtDNA is especially at risk of a free radical strike due to its proximity to where the free radicals originate from. A strike from a free radical can cause major deletions to mtDNA, eliminating a mitochondrion’s ability to assemble the proteins it needs to generate energy.

Once a mitochondrion is damaged in this way and cannot produce energy in the normal way, it enters into an abnormal metabolic state to survive. This altered state produces little in the way of energy and generates large amounts of waste that the cell cannot metabolize.

Strangely, cells tend to favor these damaged mitochondria rather than destroying and recycling them. One damaged mutant mitochondrion can quickly take over an entire cell via its progeny, and these cells dump large amounts of waste into the circulatory system, doing a disproportionate amount of damage to the body as a whole.

In 2015, the MitoSENS project was launched on Lifespan.io. This is a novel research project that aims to repair these mitochondrial mutations by creating backup copies of our mitochondrial genes in our cellular nuclei. This would offer our mtDNA the same protection that our cellular DNA enjoys, greatly improving our resistance to free radical damage.

In fact, during the course of evolution, this gradual transfer of genetic information into the nucleus has already happened with the majority of the mitochondrial genome. Nature has moved around 1000 mtDNA genes to the nucleus already, leaving behind just 13 protein-coding genes within the mitochondria.

In 2016, thanks to successful project funding on Lifespan.io, the SENS Research Foundation published the first paper demonstrating the technique was viable and showed that it had successfully migrated two mtDNA genes. Work continues on the remaining 11 genes.


[1] Boominathan, A., Vanhoozer, S., Basisty, N., Powers, K., Crampton, A. L., Wang, X., … & O’Connor, M. S. (2016). Stable nuclear expression of ATP8 and ATP6 genes rescues a mtDNA Complex V null mutant. Nucleic acids research, 44(19), 9342-9357.

Websites: The SENS Research Foundation