Melissa Trotman-Lucas, PhD
Blochet C, Buscemi L, Clément T, Gehri S, Badaut J, Hirt L. Involvement of caveolin-1 in neurovascular unit remodeling after stroke: Effects on neovascularization and astrogliosis. JCBFM. 2020;40:163-176.
Despite the collective history of failed neuroprotective therapies aimed at treating ischemic injury, the need to discover alternative stroke therapies is still present. However, despite improvements in the detection and treatment of ischemic strokes, a significant proportion of patients are ineligible for treatment and, therefore, unable to benefit. This impacts patient outcome, leaving many individuals with lifelong disabilities. Currently, the neurovascular unit (NVU) is being considered as a viable therapeutic target. This complex combination of capillaries, endothelial cells, pericytes, astrocytes and neurons closely controls connectivity between the brain and the blood. Events in the NVU contribute to cell death and neurological dysfunction during infarction, but also certain cell types within the unit have been shown to play a role in the preservation of post-stroke brain function. Endothelial cells, for instance, are key to the dynamic process of neovascularization, whereby these cells proliferate, migrate and differentiate following ischemic injury. Neovascularization is thought to be a key process in ischemia recovery, stimulating blood flow, vascular collateralization and neuroplasticity. In addition to the role of endothelial cells post-injury, astrocytes are also understood to be prominent in post-stroke recovery, transforming in the presence of molecules released during ischemic damage such as cytokines. These transformed astrocytes termed reactive astrocytes are known to be important in the formation of a glial scar that surrounds the damaged tissue. Interestingly, for some time it has been thought that the glial scar hindered axonal growth during brain recovery; however, recent evidence suggests the opposite and indeed promotion of axon development.