Fig. 1.

Pathways and mechanisms underlying the contribution of BMCs in the pathogenesis of ocular neovascularization. BMCs contribute to the development of ocular neovascularization in four phases (mobilization, migration, adhesion and differentiation), and this process is finely regulated by complex signaling pathways. Cytokines, such as VEGF and SDF-1, are involved in mobilization and migration; the adhesion of BMCs is mainly regulated by adhesion molecules including VCAM-1 and ICAM-1. However, the mechanisms regulating the differentiation of BMCs are largely unknown at present. BMCs bone marrow-derived cells, VEGF vascular endothelial growth factor, VEGFR VEGF receptor, G-CSF granulocyte colony-stimulating factor, EPO erythropoietin, HIF-1 hypoxia-inducible factor-1, SDF-1 stromal cell-derived factor-1, CXCR4 CXC receptor-4, eNOS endothelial nitric oxide synthase, MMPs matrix metalloproteinases, MkitL membrane-bound kit ligand, SkitL soluble kit ligand, EC endothelial cells, VSMCs vascular smooth muscle cells, Mφ macrophages, Ang II angiotensin II, ICAM-1 intercellular adhesion molecule-1, VCAM-1 vascular cell adhesion molecule-1