Modeling the Contribution of Cellular Senescence to the Tradeoff Between Cancer Risk and Aging

Researchers consider that the state of late life health in humans, and the mechanisms involved, are a balance between risk of death by cancer and risk of death by loss of tissue function. Cancer risk is increased by the activity of damaged cells, particularly stem cells, in a dysfunctional tissue environment, while loss of tissue function is accelerated by suppressing that activity. Tissue must be maintained, such as via a supply of new cells to replace losses, and cells must be active in order for that maintenance to occur. Cellular senescence is a part of this balance of benefit and harm. Cellular senescence is a cancer suppression mechanism, halting the replication of cells at risk of becoming cancerous, as well as attracting the attention of the immune system to the local area via inflammatory signaling. Too much cellular senescence, and a lasting burden of cellular senescence when senescent cells are not efficiently destroyed by the immune system, disrupts tissue function and accelerates degenerative aging via that very same inflammatory signaling, however. The advent of senolytic therapies to selectively destroy senescent cells will allow us to have our cake and eat it. If senescent cells are only periodically removed by treatment, then the short-term benefit of cellular senescence in suppression of immediate cancer risk resulting from cell damage will be retained, while the long-term downside of lingering senescent cells will be eliminated. Modelin...
Source: Fight Aging! - Category: Research Authors: Tags: Medicine, Biotech, Research Source Type: blogs