Role of gasotransmitters in pyroptosis

Abstract

Pyroptosis is a special form of programmed cell death. Pyroptosis is triggered by inflammasomes. The main morphological change is that the cells continue to expand until the cell membrane ruptures, and then the cell contents are released, triggering a strong inflammatory response. Investigating the molecular mechanisms of pyroptosis holds significant implications for understanding disease pathogenesis, monitoring disease progression, and developing therapeutic interventions. This review summarizes the roles of three gasotransmitters. We summarized the mechanisms of action of these three gasotransmitters in tumor diseases, inflammatory diseases, and other specific diseases. Hydrogen sulfide (H₂S), nitric oxide (NO) and carbon monoxide (CO) have dual effects on pyroptosis. They inhibit the NF-κB/NLRP3 signaling pathway, reduce the release of reactive oxygen species (ROS), and activate the nrf2 signaling pathway, thereby reducing the activation of caspase-1 and the release of other inflammatory factors, inhibiting pyroptosis and alleviating inflammatory diseases. Pyroptosis is induced and cancer cell death is promoted by increasing the expression of NLRP3, ASC, Pro-caspase-1, Cleaved-caspase-1, GSDMD, GSDMD-N and IL-1β. The significance of this study lies in revealing the mechanism of action of gasotransmitters on pyroptosis, exploring donor drugs and key enzyme inhibitors of gasotransmitters, and providing practical support for the treatment and prevention of tumor diseases, inflammatory diseases, etc. This paper reviews the latest progress of this research direction at home and abroad.

Keywords: CO; Gasotransmitter; H(2)S; NO; Pyroptosis.