Researchers recently demonstrated that they could rescue a form of mitochondrial dysfunction in mice by importing a gene from a sea squirt species. This is particularly interesting in the context of aging, as it appears to be possible to use this approach to work around any sort of damage to complexes III and IV in the mitochondrial electron transport chain (ETC). Every cell is equipped with a herd of mitochondria that act as generators, packaging the chemical energy store molecules used to power the cell. The ETC is central to this function.

The protein complexes that make up the ETC are made up of a mix of proteins encoded in both nuclear DNA and mitochondrial DNA. Dramatic mutations, such as deletions, can lead to mitochondria that function poorly or not at all. When this occurs during embryonic development, the result is either death or a much shortened and more uncomfortable life. When a mutation in mitochondrial DNA occurs in a single cell in an adult, on the other hand, as the result of the sort of random damage that takes place constantly in cells, it is usually either promptly repaired or the damaged mitochondrion is recycled.

Some forms of damage can lead to a more insidious result, however, producing a mitochondrion that is both dysfunctional and able to evade quality control mechanisms. Since mitochondria replicate like bacteria, on the rare occasions on which this happens, a cell is quickly overtaken by broken mitochondria. The cell becomes broken itself, exporting harmful oxidative molecules into the surrounding tissue and bloodstream. This has a range of undesirable downstream consequences, one of which is the creation of oxidized lipids that contribute to atherosclerosis.

The SENS Research Foundation's approach to this problem is gene therapy to place backup copies of mitochondrial genes into the better protected cell nucleus. Thus even given damage to mitochondrial DNA, there is still a supply of proteins to ensure that the ETC functions correctly. The paper here represents an alternative but conceptually similar approach, adding novel protein machinery from other species that can do some of the work of ETC protein complexes. It only fixes a portion of the lost functionality in this case, but is nonetheless most intriguing. The researchers are focused on mitochondrial disease, but it would be very interesting to repeat their approach in the context of aging and mitochondrial function.

Alternative oxidase-mediated respiration prevents lethal mitochondrial cardiomyopathy