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- W4311364326 endingPage "435" @default.
- W4311364326 startingPage "425" @default.
- W4311364326 abstract "Acetaminophen (APAP) is a widely used pain reliever that can cause liver injury or liver failure in response to an overdose. Understanding the mechanisms of APAP-induced cell death is critical for identifying new therapeutic targets. In this respect it was hypothesized that hepatocytes die by oncotic necrosis, apoptosis, necroptosis, ferroptosis and more recently pyroptosis. The latter cell death is characterized by caspase-dependent gasdermin cleavage into a C-terminal and an N-terminal fragment, which forms pores in the plasma membrane. The gasdermin pores can release potassium, interleukin-1β (IL-1β), IL-18, and other small molecules in a sublytic phase, which can be the main function of the pores in certain cell types such as inflammatory cells. Alternatively, the process can progress to full lysis of the cell (pyroptosis) with extensive cell contents release. This review discusses the experimental evidence for the involvement of pyroptosis in APAP hepatotoxicity as well as the arguments against pyroptosis as a relevant mechanism of APAP-induced cell death in hepatocytes. Based on the critical evaluation of the currently available literature and understanding of the pathophysiology, it can be concluded that pyroptotic cell death is unlikely to be a relevant contributor to APAP-induced liver injury." @default.
- W4311364326 created "2022-12-25" @default.
- W4311364326 creator A5065039252 @default.
- W4311364326 creator A5073983381 @default.
- W4311364326 creator A5087156903 @default.
- W4311364326 date "2022-12-13" @default.
- W4311364326 modified "2023-10-01" @default.
- W4311364326 title "Role of Pyroptosis in Acetaminophen-Induced Hepatotoxicity" @default.
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