Mitochondrial Epigenetics in Age-Related Mitochondrial Dysfunction

The hundreds of mitochondria present in every cell in the body undertake the essential duty of producing chemical energy store molecules, adenosine triphosphate (ATP), used to power the cell. With age, mitochondria become less efficient and more damaged, generating oxidative stress and triggering inflammation while producing less ATP than is optimal. This is thought to be a major contribution to degenerative aging, though as for all contributions to aging, it requires a highly targeted way to improve mitochondrial function in order to determine just how important it is. That highly targeted therapy doesn't yet exist in a useful form. The most plausible near future candidate is transplantation of young, functional mitochondria. Mitochondria are descended from ancient bacteria that became symbiotic with early cells. As such, they retain a small remnant circular genome, the mitochondrial DNA. In today's open access paper, researchers note that while the mitochondrial transcription machinery producing proteins from DNA sequences is different from that of the nucleus, mitochondrial DNA is still subject to epigenetic marks that can change protein output. Epigenetic patterns on the genome are known to change with age, producing changes in protein levels that are some mix of harmful and adaptive. It is reasonable to think that epigenetic regulation of protein production can be just as involved in age-related declines in the mitochondria as it is in the nucleus. Mitochon...
Source: Fight Aging! - Category: Research Authors: Tags: Medicine, Biotech, Research Source Type: blogs