Heterogeneity of cellular senescence and its implications for the development of markers

Aging is the decline in fitness that individuals suffer with time and that leads to death. Exposure to sunlight, chemicals, unhealthy food, lack of exercise and even the secondary effects of medicines can all cause damage to cells and organs. Although our cells have mechanisms to combat and repair this damage, occasionally the harm is big enough that it cannot be repaired. Some cells with unrepaired damage simply die, while others remain alive but unable to divide so they can avoid spread of the injury. These damaged but alive, are called “senescent cells”. With time, senescent cells accumulate in the organism, and become an obstacle for the regeneration of tissue eventually leading to dysfunction and aging. Furthermore, senescent cells put the immune system in permanent alert, which causes a chronic state of inflammation and eventually triggers age-related diseases. The goal of this thesis was to find genes make senescent cells different from “normal” (non-senescent) cells. We found new processes and genes that are common and we discussed their potential as novel markers for cellular senescence. However, we also highlighted the variability that exists on different types of senescence and even from one senescent cell to the other. If we were able to recognize senescent cells with adequate markers, we could either eliminate them from the body or modify them to avoid their negative effects. Preventing age-related diseases would have a positive effect in the economy and the well-being of humans.

Dissertation: http://hdl.handle.net/11370/39b8503c-1337-4e84-b789-aa96f343b555