Cellular Senescence in Aging and Cancer

Here is an open access review of what is presently known of the ways in which cellular senescence contributes to aging: "Cellular senescence is a mechanism that induces an irreversible growth arrest in all somatic cells. Senescent cells are metabolically active but lack the capacity to replicate. ... While induction of senescence is considered a major natural barrier against the uncontrolled proliferation characteristic of cancer, accumulation of senescent cells contributes to the process of aging and might promote tumor development. Senescent cells that appear to be resistant to apoptosis might be involved in the general organ dysfunction associated to aging and eventually promote cancer. It is widely accepted that the decline of organs and tissue function observed to occur with aging is associated with the accumulation of senescent cells. ... increased genomic instability is associated to inefficiency in DNA double strand repair ability of presenescent and senescent cells accumulating with aging. In addition, senescent cells might favor a [pro-cancer] tissue environment by secreting growth factors, extracellular matrix components and inflammatory cytokines that disrupt tissue integrity. Therefore, it has been suggested that senescence contributes to the process of aging and protects cells from uncontrolled growth makes it a cellular process beneficial or detrimental depending on the age of the organism. This suggests that senescence is an antagonistically pleiotropic phenomenon. For this reason senescence has been ironically defined as the Dr Jekyll and Mr. Hyde of aging." Therefore we should use targeted cell killing therapies to remove senescent cells.

Link: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2802848/

Comment Submission

Post a comment; thoughtful, considered opinions are valued. New comments can be edited for a few minutes following submission. Comments incorporating ad hominem attacks, advertising, and other forms of inappropriate behavior are likely to be deleted.

Note that there is a comment feed for those who like to keep up with conversations.