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Apoptosis is a process whereby cells activate an intrinsic cell suicide program that is one of the potential cellular responses, such as differentiation and proliferation. The number of cells in the organism is tightly regulated—not simply by controlling the rate of cell division, but also by controlling the rate of cell death. Many theories of apoptosis have been proposed, and they can be divided into intrinsic and extrinsic pathways. The intrinsic pathways including many hypothesis, and many factors involved in them, such as gene, DNA damage, some proteins, and kinases or phosphatases, lysosomes, mitochondria, persistent stress, and ROS.

In persistent stress, such as in aging, increased apoptotic resistance can lead to the survival of unfit cells that are not able to maintain proper housekeeping functions. This increase in apoptotic resistance may be relevant if one considers the context of tissue integrity during aging, but it takes place at the cost of housekeeping potential and leads to a senescent phenotype in post-mitotic cells. Cellular senescence is the state where cells have irreversibly lost their proliferation ability, and they exhibit deficiencies in maintaining their homeostatic processes. The number of senescent cells increases in tissues with aging. Age-related degeneration can be a consequence of a genetic program or it may be an entropic process. Ultimately, disorders in housekeeping ability jeopardize homeostasis and expose cells to apoptotic forms of cell death.

Accumulating evidence strongly suggests that deregulation of apoptosis is associated with the aging process, however, it is still debatable whether aging suppresses or enhances apoptosis in vivo.