Genetic removal of Nlrp3 protects against age-related and R345W Efemp1-induced basal laminar deposit formation.

ABSTRACT: Chronic, unresolved inflammation has long been speculated to serve as an initiating and propagating factor in numerous neurodegenerative diseases, including a leading cause of irreversible blindness in the elderly, age-related macular degeneration (AMD). Intracellular multiprotein complexes called inflammasomes in combination with activated caspases facilitate production of pro-inflammatory cytokines such as interleukin 1 beta. Specifically, the nucleotide-binding oligomerization (NOD)-like receptor protein 3 (NLRP3) has received heightened attention due to the wide range of stimuli to which it can respond and its potential involvement in AMD. In this study, we directly tested the role of Nlrp3 and its downstream effector, caspase 1 (Casp1) in mediating early AMD-like pathology (i.e., basa

SUBMITTER: Ortega AJ 

PROVIDER: S-EPMC12592729 | biostudies-literature | 2025 Nov

REPOSITORIES: biostudies-literature