p53 in senescence - it's a marathon not a sprint

The tumour suppressor p53, a stress-responsive transcription factor, plays a central role in cellular senescence. The role of p53 in senescence-associated stable proliferative arrest has been extensively studied. However, increasing evidence indicates that p53 also modulates the ability of senescent cells to produce and secrete diverse bioactive factors (collectively called the senescence-associated secretory phenotype, SASP). Senescence has been linked with both physiological and pathological conditions, the latter including ageing, cancer and other age-related disorders, in part through the SASP. Cellular functions are generally dictated by the expression profile of lineage-specific genes. Indeed, expression of SASP factors and their regulators are often biased by cell type. In addition, emerging evidence suggests that p53 contributes to deregulation of more stringent lineage-specific genes during senescence. P53 itself is also tightly regulated at the protein level. In contrast to the rapid and transient activity of p53 upon stress ('acute-p53'), during senescence and other prolonged pathological conditions, p53 activities are sustained and fine-tuned through a combination of different inputs and outputs ('chronic-p53').

Automated summary

The tumour suppressor p53 plays a central role in cellular senescence by regulating both senescence-associated stable proliferative arrest and the secretion of bioactive factors known as the senescence-associated secretory phenotype (SASP). Senescence is associated with various physiological and pathological conditions, including ageing, cancer, and other age-related disorders. Cell functions are determined by the expression of lineage-specific genes, which are also influenced by p53. Additionally, p53 is tightly regulated at the protein level, and its activity is sustained and fine-tuned during senescence and other prolonged pathological conditions.