Do tumor-suppressive mechanisms contribute to organism aging by inducing stem cell senescence?
J. Clin. Invest. Pier Giuseppe Pelicci, et al. 113:4 doi:10.1172/JCI20750 [
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Figure 1DNA damage accumulates as the consequence of endogenous (telomere dysfunction, oxidative stress) or exogenous (oxidative stress, γ-irradiation, UV light, and others) attacks. Damaged DNA activates checkpoint responses tRb pathways and that result in apoptosis or cellular senescence. If these events occur in stem/progenitor cells, tissue homeostasis is altered — a phenomenon that might contribute to aging. If, instead, DNA mutations that inactivate these checkpoint pathways accumulate, then cancer can arise.
