Table 3.
Study | Model/Cell type studied | Technique | Findings | Relevance of findings to pyroptosis |
---|---|---|---|---|
Chi et al. (50) | Mouse model of acute IOP-induced glaucoma | PCR, western blotting | TLR4 deficiency protected against inflammasome activation and RGC death after acute IOP elevation via caspase-1 and caspase-8-dependent pathways | Pyroptosis-associated inflammatory pathways take place and cause RGC death after acute IOP elevation |
Chi et al. (51) | Mouse model of acute IOP-induced glaucoma | PCR, western blotting | Inhibition of HMGB1, like TLR4 deficiency, protected against inflammasome activation and RGC death after acute IOP elevation via caspase-1 and caspase-8-dependent pathways | Pyroptosis-associated inflammatory pathways take place and cause RGC death after acute IOP elevation |
Qi et al. (52) | RIR injury rat model | TUNEL staining, western blotting | Inhibition of TLR4 increased RGC survival by decreasing apoptosis | TLR4-mediated pathway may lead to RGC apoptosis rather than pyroptosis after RIR injury |
Pronin et al. (53) | Acute OHT mouse model | Western blotting, immunohistochemistry | Within a few hours of inducing acute OHT in mouse eyes, retinal levels of GSDMD, caspase-1, and NLRP3 were significantly increased | Markers of GSDMD-mediated pyroptosis are upregulated in the retina after exposure to acute OHT |
Chen et al. (54) | RIR injury mouse model | HE staining, retrograde FG-labeled imaging, immunofluorescence, western blotting | Genetic deletion of GSDMD significantly increased retinal thickness and decreased RGC death after RIR injury | Absence of an effector of pyroptosis protects against RGC death after RIR injury |
Dong et al. (55) | Chronic OHT rat model | Western blotting | Protein levels of mature caspase-1 were elevated in rat retinas after chronic OHT | Caspase-1 processing, which can lead to pyroptosis, is increased in rat retinas with chronic OHT |
Zhang et al. (56) | Chronic OHT mouse model | Western blotting | Protein levels of NLRP3 and cleaved caspase-1 were elevated during the chronic OHT process | Components of the canonical pyroptotic pathway are activated in a chronic OHT mouse model |
Wan et al. (57) | RIR injury mouse model | Western blotting | RIR injury increased GSDMD-N expression in Iba-1+ microglia | An effector of pyroptosis is upregulated in microglia after RIR injury |
IOP, intra-ocular pressure; RGC, retinal ganglion cell; PCR, polymerase chain reaction; RIR, retinal ischemia/reperfusion; TUNEL, terminal deoxynucleotidyl transferase dUTP nick end labeling; OHT, ocular hypertension; HE, hematoxylin and eosin; FG, fluoro-gold; NLRP3, nucleotide-binding and oligomerization domain (NOD)-like receptor family pyrin domain-containing 3; IL-1β; interleukin-1β; IL-18, interleukin-18; GSDMD, gasdermin D; GSDMD-N, N-terminal of gasdermin D; TLR4, toll-like receptor 4; HMGB1, high-mobility group box 1.