Improving Mitochondrial Complex I Function in Aged Tissues Might Be Achieved via Upregulation of Just a Few Component Proteins

Mitochondria are the power plants of the cell, several hundred working away in every cell to package the chemical energy store molecule adenosine triphosphate (ATP). At the heart of this energetic process taking place inside every mitochondrion is the electron transport chain, consisting of several complicated protein complexes, each made up of multiple subunit proteins that are manufactured from their genetic blueprints somewhat independently of one another. Research into other complicated protein complexes, such as the proteasome, has shown that the relatively slow pace of production of one of the protein subunits can be rate-limiting to the formation of the complex as a whole. Overall function can thus be improved by increasing expression of just that one protein subunit. See the work on the β5 subunit of the fly proteasome, for example. In today's open access paper, researchers report that a similar situation may exist for complex I of the electron transport chain in mitochondria. In the past, it has been demonstrated in animal studies that impairing expression of components of complex I can produce a compensatory response that leads to improved cell function and slower pace of aging. It is perhaps the case that increased expression of some components can also achieve a slowing of aging by compensating in part for the age-related decline in mitochondrial function. This is probably not the best approach to the mitochondrial dysfunction of aging, howe...
Source: Fight Aging! - Category: Research Authors: Tags: Medicine, Biotech, Research Source Type: blogs