Sick mitochondria cause telomere damage: implications for disease

Abstract

Dysfunctional mitochondria have been implicated in a variety of human pathophysiological conditions such as cancer, neurodegeneration, and aging. However, the precise role of mitochondrial-generated reactive oxygen species (ROS) in these maladies is unclear. Using a light-activated mitochondrially targeted approach, we recently reported direct evidence that damaged mitochondria produce a wave of secondary ROS, causing rapid and preferential telomere dysfunction but not gross nuclear DNA damage (Fig 1).