Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 2024 Mar 6;17:1481–1501. doi: 10.2147/JIR.S448693

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

© 2024 Al Mamun et al.

This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License (http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms (https://www.dovepress.com/terms.php).

PMC Copyright notice

Cellular and molecular mechanisms of pyroptosis-related signaling pathways. Pyroptotic signaling pathways are mainly triggered by the stimulation of damage-associated molecular patterns (DAMPs) or pathogen-associated molecular patterns (PAMPs), leading to the activation of a variety of inflammasome components. The activated inflammasome proteins further activate the Caspase-1 pathway. Then, the activated Caspase-1 splits GSDMD to produce GSDMD N-fragment and plasma membrane pores, resulting in pyroptosis-dependent cell death. Furthermore, the Caspase-1 pathway triggers the formation and release of IL-1β and IL-18 inflammatory factors. In addition, LPS binds to the precursor of Caspase-4/5/11, inducing pyroptosis. Caspase-3/GSDME can also cause pyroptosis-mediated cell death. In addition, mitochondrial and death receptors can also trigger the Caspase-3 pathway. The activated Caspase-3 splits GSDME to produce GSDME N-fragment, creating cytoplasmic membrane pores, cell contraction and denaturation, resulting in pyroptosis-mediated cell death.