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Dr. Valery Krizhanovsky The Karl and Frances Korn |
The accumulation of damaged cells in tissues leads to tissue destruction and cancer. Elaborate mechanisms occur to limit expansion of the damaged cells and also to ensure their elimination from the tissues. Cellular senescence, a stable irreversible form of cell cycle arrest, is a mechanism which limits the proliferative potential of cells. Cellular senescence is a potent barrier to tumorigenesis and contributes to the cytotoxicity of chemotherapeutic agents. With age, senescent cells have also been observed to accumulate in human tissues.
Senescent cells present and secrete a variety of factors to their microenvironment. These factors impact a tissue homeostasis and can either interfere or support the normal function of the tissue. In order to understand the role of cellular senescence in tissue damage, cancer and aging our research aims to uncover the mechanisms of interaction of the senescent cells with their microenvironment.
| Cellular senescence limits liver fibrosis |
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 Cellular senescence of activated stellate cells limits fibrosis through a coordinated program involving cell cycle exit, down-regulation of ECM components, up-regulation of ECM-degrading enzymes, and enhanced immunosurveillance. Thus, senescence represents a homeostatic mechanism that enables the tissue to return to its pre-damaged state. Such a scheme may be broadly relevant to other wound healing responses. |