| First Author | Wooff Y | Year | 2020 |
| Journal | Sci Rep | Volume | 10 |
| Issue | 1 | Pages | 2263 |
| PubMed ID | 32041990 | Mgi Jnum | J:287378 |
| Mgi Id | MGI:6407374 | Doi | 10.1038/s41598-020-58849-z |
| Citation | Wooff Y, et al. (2020) Caspase-1-dependent inflammasomes mediate photoreceptor cell death in photo-oxidative damage-induced retinal degeneration. Sci Rep 10(1):2263 |
| abstractText | Activation of the inflammasome is involved in the progression of retinal degenerative diseases, in particular, in the pathogenesis of Age-Related Macular Degeneration (AMD), with NLRP3 activation the focus of many investigations. In this study, we used genetic and pharmacological approaches to explore the role of the inflammasome in a mouse model of retinal degeneration. We identify that Casp1/11(-/-) mice have better-preserved retinal function, reduced inflammation and increased photoreceptor survivability. While Nlrp3(-/-) mice display some level of preservation of retinal function compared to controls, pharmacological inhibition of NLRP3 did not protect against photoreceptor cell death. Further, Aim2(-/-), Nlrc4(-/-), Asc(-/-), and Casp11(-/-) mice show no substantial retinal protection. We propose that CASP-1-associated photoreceptor cell death occurs largely independently of NLRP3 and other established inflammasome sensor proteins, or that inhibition of a single sensor is not sufficient to repress the inflammatory cascade. Therapeutic targeting of CASP-1 may offer a more promising avenue to delay the progression of retinal degenerations. |
