The article discusses the role of cellular senescence in chronic inflammation and its impact on aging and age-related diseases. Cellular senescence, a tumor suppressive stress response, is associated with an increase in the secretion of pro-inflammatory proteins, contributing to chronic inflammation. The authors list the secreted factors that make up the pro-inflammatory phenotype of senescent cells and describe their effects on tissue homeostasis. They also summarize the cellular pathways and processes that regulate this phenotype, including the DNA damage response, microRNAs, key transcription factors, kinases, and chromatin remodeling. The article highlights the potential benefits and drawbacks of the senescence-associated secretory phenotype (SASP) and its role in both tumor suppression and age-related pathologies. The SASP is regulated by multiple pathways, including the DNA damage response, p38MAPK, IL-1α, and microRNAs, and global changes in chromatin organization. The authors suggest that understanding the SASP's regulation could lead to therapeutic interventions aimed at mitigating its detrimental effects without compromising its beneficial functions.The article discusses the role of cellular senescence in chronic inflammation and its impact on aging and age-related diseases. Cellular senescence, a tumor suppressive stress response, is associated with an increase in the secretion of pro-inflammatory proteins, contributing to chronic inflammation. The authors list the secreted factors that make up the pro-inflammatory phenotype of senescent cells and describe their effects on tissue homeostasis. They also summarize the cellular pathways and processes that regulate this phenotype, including the DNA damage response, microRNAs, key transcription factors, kinases, and chromatin remodeling. The article highlights the potential benefits and drawbacks of the senescence-associated secretory phenotype (SASP) and its role in both tumor suppression and age-related pathologies. The SASP is regulated by multiple pathways, including the DNA damage response, p38MAPK, IL-1α, and microRNAs, and global changes in chromatin organization. The authors suggest that understanding the SASP's regulation could lead to therapeutic interventions aimed at mitigating its detrimental effects without compromising its beneficial functions.