Cellular communication network factor 1 promotes retinal leakage in diabetic retinopathy via inducing neutrophil stasis and neutrophil extracellular traps extrusion
Neutrophil Extracellular Traps
Blood–retinal barrier
DOI:
10.1186/s12964-024-01653-3
Publication Date:
2024-05-16T09:13:42Z
AUTHORS (13)
ABSTRACT
Diabetic retinopathy (DR) is a major cause of blindness and characterized by dysfunction the retinal microvasculature. Neutrophil stasis, resulting in inflammation occlusion microvessels, key mechanism driving DR. These plugging neutrophils subsequently release neutrophil extracellular traps (NETs), which further disrupts vasculature. Nevertheless, primary catalyst for NETs extrusion microenvironment under diabetic conditions remains unidentified. In recent studies, cellular communication network factor 1 (CCN1) has emerged as central molecule modulating pathological settings. Additionally, our previous research shed light on pathogenic role CCN1 maintaining endothelial integrity. However, precise microvascular its potential interaction with have not yet been investigated.
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