Inflammatory Cytokines Induce Apoptosis of Corneal Endothelium through Nitric Oxide

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Abstract

The specific release of proinflammatory cytokines from alloreactive infiltrating cells, in combination with the inflamed environment of a corneal allograft, results in apoptosis in the corneal endothelium. This effect is mediated by the de novo generation of NO and sustained activation of NF-kappaB, p38, and STAT-1. Inflammatory cytokine-induced apoptosis presents a new target for the development of interventions to prevent or attenuate endothelial injury in graft rejection.

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