Examining the Details of Mitochondrial Dysfunction in the Aging Mouse Heart

Every cell contains hundreds of mitochondria, hard at work to produce the chemical energy store molecule adenosine triphosphate (ATP), used to power cellular activities. Mitochondria are complex structures, the evolved descendants of ancient symbiotic bacteria that are now integrated into the cell. At their center is the electron transport chain, a collection of protein complexes that conducts the energetic chemical reactions needed to make ATP. Mitochondria bear copies of a remnant circular genome, DNA distinct from that in the cell nucleus, which encodes some of the mitochondrial proteins necessary for mitochondrial function. The sequences for other mitochondrial proteins have migrated over time into the nuclear DNA. A great deal of evidence points to a significant role for mitochondrial dysfunction in degenerative aging. This arises in part due to damage to mitochondrial DNA, which is less well protected and maintained than is the case for nuclear DNA. It is also a matter of age-related changes in the expression of mitochondrial genes in the cell nucleus, which appear to affect both function of mitochondria and the clearance of damaged mitochondria via mitophagy, a form of selective autophagy. Mitochondria are dynamic organelles, constantly dividing and fusing together, and imbalances in this behavior can impair mitophagy, as well as lead to smaller numbers of mitochondria than would be optimal. Today's open access paper takes a look at the proximate outcomes...
Source: Fight Aging! - Category: Research Authors: Tags: Medicine, Biotech, Research Source Type: blogs