摘要：Cellular senescence is a stable form of cell cycle arrest that limits the propagation of damaged cells and can be triggered in response to diverse forms of cellular stress [1]. This anti-proliferative program is mediated by the p53 and Rb pathways and was initially considered a cell-autonomous mechanism that promotes tumor suppression and tissue homeostasis [1]. However, several groundbreaking studies performed in the last decade have established that senescent cells can impact their environment through the secretion of growth factors, cytokines, chemokines, immune modulators and extracellular matrix-degrading enzymes [1]. This process, collectively known as the senescence- associated secretory phenotype (SASP), enables the non-cell-autonomous activities of senescent cells. The functions exerted by the SASP are diverse and include the autocrine reinforcement of cell cycle arrest as well as the paracrine transmission of the senescent phenotype to neighboring cells, thereby maintaining and propagating tumor suppression [1]. Moreover, SASP can directly modulate the tissue microenvironment, elicit immune surveillance of senescent cells, and paradoxically, promote tumorigenesis by supporting the proliferation of surrounding malignant or pre-malignant cells [1].
