Abstract:Corneal transparency depends on an avascular microenvironment, regularly organized stromal collagen, and regulated inflammatory repair response.CD34+ cells should not be regarded as a single functional population; rather, they comprise cornea-resident mesenchymal stem cell-like cells, peripheral blood-derived endothelial progenitor cells(EPCs), and fibrocytes with distinct origins, phenotypes, and pathological effects. Resident CD34+ cells are mainly associated with limbal stem cell niche maintenance and stromal homeostasis, whereas recruited EPCs and fibrocytes may contribute to corneal neovascularization and scarring under hypoxic, inflammatory, or TGF-β-driven conditions. This review summarizes the biological characteristics, corneal distribution, and key signaling pathways of CD34+ cells, including VEGF/VEGFR-2, SDF-1/CXCR4, NF-κB, and TGF-β/Smad signaling. And further discuss their roles in infectious keratitis, limbal stem cell deficiency, keratoconus, and post-traumatic corneal fibrosis. By integrating controversial findings with clinical evidence and translational limitations, this review suggests that future CD34-related therapies should shift from non-selective CD34 modulation toward spatiotemporally precise strategies that preserve resident reparative subpopulations while inhibiting recruited proangiogenic and profibrotic cells.
