期刊
SCIENTIFIC REPORTS
卷 10, 期 1, 页码 -出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/s41598-020-58849-z
关键词
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资金
- Ophthalmic Research Institute of Australia
- National Health and Medical Research Council of Australia [NHMRC: 1127705, APP1141504, APP1146864, APP1162103, APP1163358]
- ANU Translational Fellowship
- Australian National University
- Gretel and Gordon Bootes Medical Research Foundation
- R.D. Wright Career Development Fellowship [APP1162025]
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.
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