CORDIS Project
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This project investigates the role of mitochondrial DNA in cellular senescence and its impact on the inflammatory response associated with aging. The goal is to identify mechanisms that could lead to new therapeutic targets for controlling harmful effects of senescent cells.
In response to various stresses such as DNA damage, telomere erosion, or oncogene activation, human cells can enter senescence.
This process is characterized by irreversible proliferative arrest, deep transcriptional reprogramming, and expression of a collection of inflammatory factors termed the SASP (senescence-associated secretory phenotype).
As it limits the proliferation of cells potentially bearing neoplastic potential, the triggering of cellular senescence is an essential tumor suppressin…
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