Failing Mitophagy in the Aging Heart

Every cell contains hundreds of mitochondria, bacteria-like organelles that work to provide the cell with adenosine triphosphate (ATP), a chemical energy store molecule to power cellular biochemistry. With age, mitochondrial function falters throughout the body. This may be largely a consequence of failing mitophagy, a form of the cellular maintenance process of autophagy that is responsible for destroying worn and damaged mitochondria. In tissues with high energy demands, such as the heart, this loss of function is a sizable contributing factor in the development of age-related disease. At present the research and development communities are still in the comparatively early stages in the production of ways to address this problem. Both upregulation of NAD+ in mitochondria and delivery of mitochondrially targeted antioxidants appear to somewhat reverse the loss of mitophagy, and thus improve mitochondrial function, but the outcomes in human trials and animal models are not reliably positive at this point in time. The effect size of these treatments is likely not large enough. A range of better approaches lie ahead, such as periodic delivery of large numbers of whole mitochondria harvested from cell cultures, but even these classes of treatment do not address the root causes of mitochondrial decline. Researchers have identified a number of proteins important to mitophagy wherein expression changes with age, but connecting these changes to the underlying damage th...
Source: Fight Aging! - Category: Research Authors: Tags: Medicine, Biotech, Research Source Type: blogs