Molecular and cellular mechanisms underlying the role of blood vessels in spinal cord injury and repair.

Spinal cord injury causes immediate damage of nervous tissue accompanied by the loss of motor and sensory function. The limited self-repair ability of damaged nervous tissue underlies the need for reparative interventions to restore function after spinal cord injury. Blood vessels play a crucial role in spinal cord injury and repair. Injury-induced loss of local blood vessels and a compromised blood-brain barrier contribute to inflammation and ischemia and thus to the overall damage to the nervous tissue of the spinal cord. Lack of vasculature and leaking blood vessels impede endogenous tissue repair and limit prospective repair approaches. A reduction of blood vessel loss and the restoration of blood vessels so that they no longer leak might support recovery from spinal cord injury. The promotion of new blood vessel formation (i.e., angio- and vasculogenesis) might aid repair but also incorporates the danger of exacerbating tissue loss and thus functional impairment. The delicate interplay between cells and molecules that govern blood vessel repair and formation determines the extent of damage and the success of reparative interventions. This review deals with the cellular and molecular mechanisms underlying the role of blood vessels in spinal cord injury and repair.