CCL2 and hypoxia: Locally, retinal hypoxia leads to the release of many molecules in the vitreous, including proinflammatory cytokines [TNF-α, interleukin-1β (IL-1β), IL-6, interleukin-8 (IL-8), and interferon-γ (IFN-γ), etc.), chemokines [monocyte chemoattractant protein-1 (MCP-1)], growth factor (VEGF, FGF, and PDGF etc.), adhesion molecules [ICAM-1 and vascular cellular adhesion molecules-1 (VCAM-1)], and receptors (CD40 and Toll-like receptors), from retinal vascular cells, inflammatory cells, and/or glial cells (72, 73).