Innate immune sensing of cytosolic chromatin fragments through cGAS promotes senescence. Senescent cells secrete inflammatory factors, known as the senescence-associated secretory phenotype (SASP), which influence biological processes. This study shows that the cGAS-STING pathway is involved in regulating senescence and the SASP. cGAS recognizes cytosolic chromatin fragments (CCFs) in senescent cells, activating STING and promoting SASP factors, which in turn promote paracrine senescence. The study demonstrates that various stimuli of cellular senescence engage the cGAS-STING pathway in vitro and in vivo. Deficiency of the cGAS-STING pathway impairs oxidative-stress induced senescence. The cGAS-STING pathway promotes senescence in a paracrine manner by regulating the SASP. CCFs are recognized by cGAS in senescent cells, and the degradation of nuclear envelope components leads to the release of chromatin into the cytosol, activating cGAS. Diverse triggers of cellular senescence engage the cGAS-STING pathway. cGAS regulates cellular senescence in vivo, as shown by experiments with irradiation and oncogene-induced senescence. The study highlights the role of innate DNA sensing through the cGAS-STING pathway in the regulation of senescence and the SASP. The findings provide insights into the mechanisms underlying cellular senescence.Innate immune sensing of cytosolic chromatin fragments through cGAS promotes senescence. Senescent cells secrete inflammatory factors, known as the senescence-associated secretory phenotype (SASP), which influence biological processes. This study shows that the cGAS-STING pathway is involved in regulating senescence and the SASP. cGAS recognizes cytosolic chromatin fragments (CCFs) in senescent cells, activating STING and promoting SASP factors, which in turn promote paracrine senescence. The study demonstrates that various stimuli of cellular senescence engage the cGAS-STING pathway in vitro and in vivo. Deficiency of the cGAS-STING pathway impairs oxidative-stress induced senescence. The cGAS-STING pathway promotes senescence in a paracrine manner by regulating the SASP. CCFs are recognized by cGAS in senescent cells, and the degradation of nuclear envelope components leads to the release of chromatin into the cytosol, activating cGAS. Diverse triggers of cellular senescence engage the cGAS-STING pathway. cGAS regulates cellular senescence in vivo, as shown by experiments with irradiation and oncogene-induced senescence. The study highlights the role of innate DNA sensing through the cGAS-STING pathway in the regulation of senescence and the SASP. The findings provide insights into the mechanisms underlying cellular senescence.