Targeting pyroptosis in inflammatory bowel disease: A potentially effective therapeutic approach

Figure 1 Canonical and non-canonical activation pathways of pyroptosis. NLRP3: Nucleotide-binding oligomerization domain-like receptor family pyrin domain-containing 3; PAMP: Pathogen-associated molecular pattern; DAMP: Damage-associated molecular pattern; LPS: Lipopolysaccharide; TLR: Toll-like receptor; NF-κB: Nuclear factor kappa-B; ASC: Adapter protein apoptosis-associated speck-like protein containing a CARD; HAMP: Homeostasis-altering molecular processes; ROS: Reactive oxygen species; mtDNA: Mitochondrial DNA; IL: Interleukin.

Figure 2 The pathogenic role of pyroptosis in inflammatory bowel disease. DAMP: Damage-associated molecular pattern; IL: Interleukin; ZO-1: Zonula occludens-1; NE: Neutrophil elastase cell; M: Membranous/microfold cell; DC: Dendritic cell; IEC: Intestinal epithelial cell.

Figure 3 Research progress on pyroptosis inhibitors for inflammatory bowel disease treatment. IBD: Inflammatory bowel disease; siRNA: Small interfering RNA.

Figure 4 Targeting the nucleotide-binding oligomerization domain-like receptor family pyrin domain-containing 3 inflammasome pathway: Mechanisms and therapeutic inhibitors. NLRP3: Nucleotide-binding oligomerization domain-like receptor family pyrin domain-containing 3; IL: Interleukin; TLR: Toll-like receptor; NF-κB: Nuclear factor kappa-B; GSDMD: Gasdermin D; IL-1R: Interleukin-1 receptor; IL-18R: Interleukin-18 receptor; ASC: Adapter protein apoptosis-associated speck-like protein containing a CARD; ASO: Antisense oligonucleotide; siRNA: Small interfering RNA.