Cellular and molecular mechanisms in vascular repair after traumatic brain injury: a narrative review

Traumatic brain injury (TBI) disrupts normal brain function and is associated with high morbidity and fatality rates. TBI is characterized as mild, moderate or severe depending on its severity. The damage may be transient and limited to the dura matter, with only subtle changes in cerebral parenchyma, or life-threatening with obvious focal contusions, hematomas and edema. Blood vessels are often injured in TBI. Even in mild TBI, dysfunctional cerebral vascular repair may result in prolonged symptoms and poor outcomes. Various distinct types of cells participate in vascular repair after TBI. A better understanding of the cellular response and function in vascular repair can facilitate the development of new therapeutic strategies. In this review, we analyzed the mechanism of cerebrovascular impairment and the repercussions following various forms of TBI. We then discussed the role of distinct cell types in the repair of meningeal and parenchyma vasculature following TBI, including endothelial cells, endothelial progenitor cells, pericytes, glial cells (astrocytes and microglia), neurons, myeloid cells (macrophages and monocytes) and meningeal lymphatic endothelial cells. Finally, possible treatment techniques targeting these unique cell types for vascular repair after TBI are discussed.

Automated summary

Traumatic brain injury (TBI) disrupts normal brain function and can have serious consequences. Blood vessels are often damaged in TBI, leading to impaired cerebral vascular repair, which can result in prolonged symptoms and poor outcomes. Understanding the cellular response and function in vascular repair after TBI is crucial for developing new therapeutic strategies. This review discusses the mechanisms of cerebrovascular impairment following TBI and the role of different cell types in vascular repair, as well as potential treatment techniques targeting these cells.