Gut vascular barrier in the pathogenesis and resolution of Crohn's disease: A novel link from origination to therapy

The gut vascular barrier (GVB) is the deepest layer of the gut barrier. It mainly comprised gut vascular endothelial cells, enteric glial cells, and pericytes. The GVB facilitates nutrient absorption and blocks bacterial translocation through its size-restricted permeability. Accumulating evidence suggests that dysfunction of this barrier correlates with several clinical pathologies including Crohn's disease (CD). Significant progress has been made to elucidate the mechanism of GVB dysfunction and to confirm the participation of disrupted GVB in the course of CD. However, further analyses are required to pinpoint the specific roles of GVB in CD pathogenesis. Many preclinical models and clinical trials have demonstrated that various agents are effective in protecting the GVB integrity and thus providing a potential CD treatment strategy. Through this review, we established a systemic understanding of the role of GVB in CD pathogenesis and provided novel insights for GVB-targeting strategies in CD treatment.

Automated summary

The gut vascular barrier (GVB) is composed of gut vascular endothelial cells, enteric glial cells, and pericytes and plays a crucial role in nutrient absorption and preventing bacterial translocation. Dysfunction of the GVB has been correlated with various clinical pathologies, including Crohn's disease (CD). Extensive research has been carried out to understand the mechanisms of GVB dysfunction and its involvement in CD, but further analysis is needed to elucidate the specific roles of GVB in CD pathogenesis. Many studies have shown the effectiveness of different agents in protecting GVB integrity, offering potential treatment strategies for CD.