Abstract
Depression and cardiovascular disease (CVD) frequently coexist, significantly impacting patient prognosis and quality of life. Research indicates that inflammatory responses play a crucial role in the pathogenesis of both conditions. The NLRP3 inflammasome, a key inflammatory signaling platform of the innate immune system, mediates the maturation and release of IL-1β and IL-18 and induces pyroptosis, playing a significant role in both depression and CVD. To explore the mechanisms and therapeutic potential of the NLRP3 inflammasome in the comorbidity of depression and CVD, we systematically reviewed recent literature. Our focus was on its activation pathways, expression changes in animal models and clinical samples, and intervention studies. The results indicate that NLRP3 inflammasome is persistently activated in patients with both depression and CVD, and this activation correlates with disease severity. Furthermore, various pharmaceutical drugs and natural compounds have demonstrated synergistic effects by inhibiting the NLRP3 inflammasome pathway. In conclusion, the NLRP3 inflammasome represents a critical molecular mechanism linking depression and CVD, as well as a potential target for combined therapeutic strategies. This area holds significant research and clinical translational value.