More Mitochondrial Fission Improves Mitophagy, Mitochondrial Function, and Angiogenesis

Mitochondria are essential cell components that become dysfunctional with age, a cause of a significant fraction of age-related degeneration. These organelles are descended from ancient symbiotic bacteria, and the herd of mitochondria in a cell is dynamic, fusing together, splitting apart, and passing around component parts. As mitochondria become worn and damaged, they are removed by the quality control process of mitophagy. This all works well in youth. In the context of aging, a fair amount of evidence points to impaired mitochondrial fission as an important contributing cause of impaired mitophagy, which in turn leads to impaired mitochondrial function as damaged mitochondria accumulate, which in turn causes all sorts of issues. The issue in question here is the reduced generation of new blood vessels with age, an impairment that may be very significant, as it contributes to the decline of capillary networks throughout the body and reduced blood supply to energy-hungry organs such as muscles and the brain. The protein Drp1 is best known to enable an orderly splitting, or fission, of mitochondria so that one becomes two and/or mitophagy, which is trimming off dysfunctional parts of existing mitochondria and helping eliminate mitochondria that are beyond repair. Researchers now have early evidence that when oxygen levels are low in common problems like heart disease and peripheral artery disease in the legs, Drp1 gets modified and a new job. It again promote...
Source: Fight Aging! - Category: Research Authors: Tags: Daily News Source Type: blogs