The decline of cell division potential of primary human cells in culture known as cellular senescence has served as a paradigm to study aging at a cellular level. Senescent cells cannot divide and therefore are incapable to contribute to normal tissue renewal. The mechanisms that maintain these cells in a state of permanent cell cycle arrest involve DNA damage, mitochondrial dysfunction and tumor suppressor genes. Senescent cells, DNA damage signals and high expression of tumor suppressors can also be detected in old organisms but their origin in vivo remains a major enigma. Independent of their origin, senescent cells have a very active metabolism and secrete a wide variety of cytokines that may have a huge impact in tissue physiology. Since senescence could be triggered by cytokines secreted by senescent cells the process can propagate and self amplify with age. We discuss a model where different pro-senescent signals are linked in positive feedback loops and controlled by negative feedback loops. We propose that aging favors the positive feedback interactions and/or inhibit the negative feedback controls.