Senescence, the process whereby cells stop dividing and tissue reveals physical signs of deterioration, is rooted in complex molecular pathways that have remained difficult to elucidate.  Thomas von Zglinicki, from Newcastle University (United Kingdom), in conjunction with an international collaboration of colleagues, investigated why cells become senescent.  The team found that when an aging cell detects serious DNA damage resulting from general wear, it prompts long-term activation of the checkpoint gene CDKN1A (p21), which induces mitochondrial dysfunction and production of reactive oxygen species (ROS); this in-turn prompts cells to self-destruct or stop dividing.  Referring to this process as a “dynamic feedback loop” the researchers write that: “We show that this loop is both necessary and sufficient for the stability of growth arrest during the establishment of the senescent phenotype.” They speculate these insights could offer explanations of the aging process and perhaps provide targeted pathways through which diseases may be more effectively addressed.