Now that the accumulation of senescent cells is broadly accepted to be one of the fundamental causes of aging, ever greater funding is flowing into this part of the scientific ecosystem. Many research groups are investigating aspects of the biochemistry of cellular senescence: how cells become senescent; the harmful signaling they produce; ways to prompt them to self-destruct, thereby removing their contribution to the aging process. One of the results of this expansion of effort is that some proteins previously known to be associated with aging are now being found to either influence or act through cellular senescence. The research here is an interesting example of the type, in which TXNIP, a protein associated with oxidative stress and aging in flies, is now implicated in cellular senescence in mice.
Cells are constantly exposed to metabolic stress, a major cause of cellular senescence. Recent reports have shown that metabolic changes influence aging in model systems, from the budding yeast to mouse models. One of the prominent cellular senescence markers is the accumulation of reactive molecules, such as reactive oxygen species (ROS), a product of an essential energy production.