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Removing nondividing, senescent cells in mice delays age-related disease

November 2, 2011


Researchers at the Mayo Clinic in Rochester, MN have found a causal relationship between senescent cells and certain age-related diseases in a mouse model, according to a report in Nature. While research on cell cultures has long suggested that senescent cells have a role in aging, the nature of this connection in live animals was less clear. The new finding suggests that cell senescence may be a fundamental mechanism that drives aging. The study was supported in part by the NIA.

In cell senescence, the cell turns off its capacity to produce new cells. This typically happens after a cell has divided so many times that it is in jeopardy of becoming abnormal and potentially dangerous. Thus, cell senescence is considered an anti-cancer mechanism. But the senescent cell, although different from its earlier self, is still alive and it works on many levels, by both sending and receiving signals.

In the Mayo Clinic study, researchers designed a process to eliminate all senescent cells in a strain of mice. Removing senescent cells delayed the onset of disease-related changes in fat tissue, skeletal muscle, and eye tissue. In addition, removing senescent cells later in the life of the mice was found to slow the progression of already established age-related disorders. 

Reference: Baker DJ, et al. Clearance of p16Ink4a-positive senescent cells delays aging-associated disorders. Nature. 2011 Nov 2;479(7372):232-6.

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