CXCR3 deletion aggravates corneal neovascularization in a corneal alkali-burn model.

ABSTRACT: Corneal neovascularization can cause devastating consequences including vision impairment and even blindness. Corneal inflammation is a crucial factor for the induction of corneal neovascularization. Current anti-inflammatory approaches are of limited value with poor therapeutic effects. Therefore, there is an urgent need to develop new therapies that specifically modulate inflammatory pathways and inhibit neovascularization in the cornea. The interaction of chemokines and their receptors plays a key role in regulating leukocyte migration during inflammatory response. CXCR3 is essential for mediating the recruitment of activated T cells and microglia/macrophages, but the role of CXCR3 in the initiation and promotion of corneal neovascularization remains unclear. Here, we showed that the ex

SUBMITTER: Li S 

PROVIDER: S-EPMC10191246 | biostudies-literature | 2022 Dec

REPOSITORIES: biostudies-literature