NOD1 deficiency ameliorates the progression of diabetic retinopathy by modulating bone marrow–retina crosstalk

• NOD1 deficiency in diabetic mice ameliorates diabetic retinopathy by restoring bone marrow hematopoietic balance and reducing retinal inflammation. • Hematopoietic-specific NOD1 ablation reduces macrophage infiltration and CXCL1/CXCL2 secretion in the retina, limiting neutrophil chemoattraction and NETosis. • Targeting NOD1 in bone marrow represents a novel therapeutic strategy for preventing and treating diabetic retinopathy. • The study reveals a critical role for NOD1 in mediating bone marrow–retina crosstalk, linking systemic innate immunity to local retinal pathology.