Chronic inflammation is closely linked to aging and contributes to age-related diseases such as cancer, atherosclerosis, and osteoarthritis. While immune cell activation is often considered the source of chronic inflammation, recent studies suggest that cellular senescence, a tumor-suppressive process, also plays a significant role by increasing the secretion of pro-inflammatory factors. Senescent cells secrete a variety of factors, collectively known as the senescence-associated secretory phenotype (SASP), which can disrupt tissue homeostasis and contribute to chronic inflammation. The SASP is regulated by several pathways, including the DNA damage response, p38MAPK, and IL-1α, and involves transcription factors such as NF-κB and C/EBPβ. MicroRNAs like miR-146a/b also modulate SASP activity by inhibiting NF-κB. Chromatin remodeling is another key aspect of SASP regulation, as senescent cells undergo structural changes that may influence gene expression. The SASP has both beneficial and harmful effects, including promoting tumor suppression and contributing to chronic inflammation. Understanding the mechanisms that regulate the SASP is crucial for developing therapies that mitigate its harmful effects without compromising its tumor-suppressive functions. The interplay between senescence and chronic inflammation highlights the complexity of aging and age-related diseases, and further research is needed to explore potential therapeutic strategies.Chronic inflammation is closely linked to aging and contributes to age-related diseases such as cancer, atherosclerosis, and osteoarthritis. While immune cell activation is often considered the source of chronic inflammation, recent studies suggest that cellular senescence, a tumor-suppressive process, also plays a significant role by increasing the secretion of pro-inflammatory factors. Senescent cells secrete a variety of factors, collectively known as the senescence-associated secretory phenotype (SASP), which can disrupt tissue homeostasis and contribute to chronic inflammation. The SASP is regulated by several pathways, including the DNA damage response, p38MAPK, and IL-1α, and involves transcription factors such as NF-κB and C/EBPβ. MicroRNAs like miR-146a/b also modulate SASP activity by inhibiting NF-κB. Chromatin remodeling is another key aspect of SASP regulation, as senescent cells undergo structural changes that may influence gene expression. The SASP has both beneficial and harmful effects, including promoting tumor suppression and contributing to chronic inflammation. Understanding the mechanisms that regulate the SASP is crucial for developing therapies that mitigate its harmful effects without compromising its tumor-suppressive functions. The interplay between senescence and chronic inflammation highlights the complexity of aging and age-related diseases, and further research is needed to explore potential therapeutic strategies.