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CD36-mediated lipid-accumulation in reactive microglia drives retinal degeneration through Nlrp3-IL-1β pathway

ABSTRACT: Lipid accumulation in microglia through CD36 enhances Nlrp3 inflammasome activation, contributing to retinal neurodegeneration.

ORGANISM(S): Mus musculus

PROVIDER: GSE324526 | GEO | 2026/07/26

REPOSITORIES: GEO

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CD36-mediated lipid-accumulation in reactive microglia drives retinal degeneration through Nlrp3-IL-1β pathway

Project description:Lipid accumulation in microglia through CD36 enhances Nlrp3 inflammasome activation, contributing to retinal neurodegeneration.

2026-07-26 | GSE333417 | GEO

CD36-mediated lipid-accumulation in reactive microglia drives retinal degeneration through Nlrp3-IL-1β pathway [CD36cko_smart_seq]

Project description:Lipid accumulation in microglia through CD36 enhances Nlrp3 inflammasome activation, contributing to retinal neurodegeneration.

2026-07-26 | GSE301932 | GEO

CD36-mediated lipid-accumulation in reactive microglia drives retinal degeneration through Nlrp3-IL-1β pathway [scRNA-seq]

Project description:Lipid accumulation in microglia through CD36 enhances Nlrp3 inflammasome activation, contributing to retinal neurodegeneration.

2026-07-26 | GSE301934 | GEO

CD36-mediated lipid-accumulation in reactive microglia drives retinal degeneration through NLRP3-IL-1β pathway

Project description:Microglia are central regulators of retinal immune homeostasis, yet their dysregulated responses can trigger neuroinflammation and drive retinal degeneration, a leading cause of irreversible blindness with limited therapeutic options. The specific pathogenic subsets and underlying mechanisms remain poorly defined. In this study, using single-cell RNA sequencing and spatial transcriptomics, we identified a distinct subset of lipid-accumulated reactive microglia (aLARM), predominantly localized to the ventral inferior retina in NaIO3-induced retinal degeneration mice, a region partially analogous to the human macula in terms of its susceptibility to neurodegenerative injury. In both patients and mouse models, this aLARM uniquely expresses high levels of CD36, which is critical for their formation and pathogenic function. Importantly, microglia-specific CD36 deletion abolished the aLARM-mediated retinal inflammation and degeneration, while subretinal transplantation of isolated CD36+ aLARM exacerbated the destruction of retinal structures and functional impairment. Furthermore, these aLARM subsets exhibited NLRP3 inflammasome activation and IL-1β production, which would activate IL-1R1 on microglia/macrophages and pericytes/ smooth muscle cells, amplifying a feed-forward inflammatory loop that worsened neurodegeneration. Finally, therapeutic blockade of CD36 using by the neutralizing antibody FA6-152 effectively reduced aLARM formationand protected against retinal degeneration. Together, our findings highlight CD36+ aLARM as a novel and targetable pathogenic microglial population that linksneuroinflammation to retinal degeneration, providing a potential foundation for microglia-based precision therapies in retinal degenerative disorders.

2026-07-26 | GSE324535 | GEO

CD36-mediated lipid-accumulation in reactive microglia drives retinal degeneration through NLRP3-IL-1β pathway

Project description:CD36-mediated lipid-accumulation in reactive microglia drives retinal degeneration through NLRP3-IL-1β pathway

| PRJNA1435759 | ENA

CD36-mediated lipid-accumulation in reactive microglia drives retinal degeneration through Nlrp3-IL-1β pathway

Project description:CD36-mediated lipid-accumulation in reactive microglia drives retinal degeneration through Nlrp3-IL-1β pathway

| PRJNA1435755 | ENA

CD36-mediated lipid-accumulation in reactive microglia drives retinal degeneration through Nlrp3-IL-1β pathway

Project description:CD36-mediated lipid-accumulation in reactive microglia drives retinal degeneration through Nlrp3-IL-1β pathway

| PRJNA1471047 | ENA

CD36-mediated lipid-accumulation in reactive microglia drives retinal degeneration through Nlrp3-IL-1β pathway [CD36cko_smart_seq]

Project description:CD36-mediated lipid-accumulation in reactive microglia drives retinal degeneration through Nlrp3-IL-1β pathway [CD36cko_smart_seq]

| PRJNA1287750 | ENA

CD36-mediated lipid-accumulation in reactive microglia drives retinal degeneration through Nlrp3-IL-1β pathway [scRNA-seq]

Project description:CD36-mediated lipid-accumulation in reactive microglia drives retinal degeneration through Nlrp3-IL-1β pathway [scRNA-seq]

| PRJNA1287754 | ENA

C-reactive protein promotes diabetic kidney disease via Smad3 mediated NLRP3 inflammasome activation

Project description:Diabetic kidney disease (DKD) is the leading cause of end-stage kidney diseases resulting enormous social-economic burden. Accumulated evidence has indicated that C-reactive protein (CRP) exacerbates DKD by enhancing renal inflammation and fibrosis through TGF-β/Smad3 signaling. NLRP3 inflammasome is the key sensor contributing to renal inflammation. However, whether CRP enhances inflammation in DKD via NLRP3 inflammasome related pathway remains unknown. In this study, we demonstrate that CRP promotes DKD via Smad3-mediated NLRP3 inflammasome activation as mice overexpressing human CRP gene exhibits accelerated renal inflammation in diabetic kidneys, which is associated with the activation of Smad3 and NLRP3 inflammasome. In contrast, blockade of CPR signaling with a neutralizing anti-CD32 antibody attenuates CRP-induced activation of Smad3 and NLRP3 in vitro. Importantly, genetic deletion or pharmacological inhibition of Smad3 also mitigates CRP-induced activation of NLRP3 in diabetic kidneys or in high glucose treated cells. Mechanistically, we reveal that Smad3 binds to the NLRP3 gene promoter which is enhanced by CRP. Taken together, we conclude that CRP induces renal inflammation in DKD via to the Smad3-NLRP3 inflammasome-dependent mechanism. Thus, targeting CRP or Smad3-NLRP3 pathways may be a new therapeutic potential for DKD.

2025-01-29 | GSE271870 | GEO

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