J. F. Passos et al., "Mitochondrial dysfunction accounts for the stochastic heterogeneity in telomere-dependent senescence," PLoS Biology, 5:1138, 2007. (Cited in 31 papers)
To investigate why cells senesce at different rates, Thomas von Zglinicki of the University of Newcastle and colleagues examined mitochondrial dysfunction in cultured fibroblasts. They found that reactive oxygen species (ROS) were produced by mitochondria in senescent cells. This ROS boost caused telomere shortening, a hallmark of cellular senescence; conversely, reducing ROS production delayed the cells' senescence.
Von Zglinicki's "was one of the first labs to show the effects of oxidative stress on telomere length," says Gordon Lithgow of the Buck Institute for Age Research in Novato, Calif. This was thought to be a cell-autonomous mechanism, but this paper "adds another dimension to what might drive telomere shortening," says Judy Campisi, also of the Buck Institute, by showing that "that ROS can also come from within the ...
