Mitochondrial Dysfunction and its Interaction with Cellular Senescence

Aging is caused by a number of independent issues, forms of damage and dysfunction that arise as a consequence of the normal operation of a youthful and undamaged metabolism. If these processes remained independent, aging would be a far less challenging field of study than is the case, but unfortunately, everything interacts with everything else in cellular biology. Processes of damage encourage one another, and combine in complex ways to produce shared consequences. Those consequences can in turn interact with the underlying mechanisms of damage to alter and accelerate their effects. In today's open access paper, researchers discuss some of the interactions between cellular senescence and mitochondrial dysfunction, two quite different mechanisms of aging. Mitochondrial dysfunction is known to promote inflammatory signaling, such as via the mislocalization of mitochondrial DNA to places in which it will trigger an innate immune response. Evidence suggests that this sort of mechanism likely drives some fraction of the harmful inflammatory signaling that is produced by senescent cells. This raises interesting questions, such as whether or not strategies intended to reverse mitochondrial dysfunction will, as a side-effect, also reduce the contribution of senescent cells to degenerative aging. Targeting Mitochondria to Control Ageing and Senescence Ageing is associated with increased inflammation and activation of the innate immune system. This condition is...
Source: Fight Aging! - Category: Research Authors: Tags: Medicine, Biotech, Research Source Type: blogs