Figure 1.

Schematic of the multicellular interactions that mediate the transition from injury into repair in the neurovascular unit. During injury and disease, the BBB is leaky, inflammation is damaging, and neurotoxicity predominates. But during repair, endogenous mechanisms are activated that involve angiogenesis and neurogenesis, trophic glial reactions, and recruitment of beneficial aspects of inflammation and remodeling. In this simplified schematic, we only depict neurons, astrocytes, microglia and endothelium. Of course, recovery after CNS injury will also involve many other cell types including pericytes, smooth muscle cells, oligodendrocytes, infiltrating or resident immune cells as well as systemic responses in other organs. Ultimately, cell–cell signaling between all elements of the neurovascular unit is required to support neural plasticity and functional compensation and recovery.