Abstract

Cell death is one of the inevitable life activities of cells during the growth and development of the body. Regulated cell death (RCD) is a type of cell death mode that can be regulated and depends on specific molecular mechanisms which play an essential role in various pathophysiological environments. Pyrolysis is a newly discovered method of programmed cell death mediated by members of the Gasdermin protein family which is characterized by the activation of inflammatory factors and the formation of cell membrane pores. The specific manifestations are the swelling of cells, the appearance of plasma membrane bullae and the release of cell contents after cell rupture. A cascade of inflammation occurs after cell death. Activation of inflammasomes activates the classic pyrolysis pathway depending on caspase-1 or the non-classical pyrolysis pathway depending on Caspase-4/5 /11 and the subsequent inflammation reaction, excessive immune response caused by microbial infection and danger signals can lead to a variety of inflammatory diseases. In the inflammatory response, large numbers of inflammasomes activate the substrate protein GSDMD. GSDMD mediates pyrolysis by forming pores in the plasma membrane and mitochondria. Many studies have shown that pyrolysis plays an essential role in inflammatory bowel disease and other inflammatory diseases. This article aims to elaborate on the molecular mechanisms of pyroptosis in ulcerative colitis (UC) pathogenesis and provide new therapeutic ideas for UC.

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