SLIT3 is a secreted guidance molecule that plays critical roles in bone homeostasis, cardiovascular function, and kidney disease. In skeletal tissue, SLIT3 is produced by osteoblasts and acts as a proangiogenic factor that promotes CD31hiEMCNhi endothelium formation, which is essential for bone formation 1. SLIT3 couples angiogenesis and osteogenesis through type H blood vessels, with its deletion resulting in low bone mass due to impaired bone formation 12. In cardiac tissue, SLIT3 is secreted by stromal cells including fibroblasts and vascular mural cells, and signals through ROBO1 receptors on cardiomyocytes to regulate pressure overload-induced cardiac hypertrophy 3. The SLIT3-ROBO1 axis promotes cardiomyocyte hypertrophy and adverse cardiac remodeling under stress conditions 3. In kidney disease, SLIT3 expression is elevated in diabetic kidney disease and serves as a potential diagnostic biomarker associated with immune cell infiltration 4. Additionally, SLIT3 functions in glomerular injury, with mesangial cell-derived SLIT3 potentially activating ROBO receptors in podocytes and endothelial cells during IgA nephropathy 5. Therapeutically, recombinant SLIT3 administration can enhance bone fracture healing and counteract osteoporotic bone loss 1.