High-throughput gene expression profiling of ischemic retinal ganglion cells (RGCs) 24 hours after reperfusion

Retinal ischemia-reperfusion (IR) is a common mechanism in numerous ocular disorders (glaucoma, diabetic retinopathy, ischemic optic neuropathy, etc.), the ultimate consequence of which is retinal ganglion cell (RGC) death, leading to visual impairment or even blindness. Currently, our ability to regulate retinal IR pathogenesis remains roughly limited to slowing the rate of degenerative change. The development of novel therapies to halt or reverse retinal degeneration will require a far deeper understanding of the molecular mechanisms involved in IR-induced RGC death. The objective of this study was to identify the activity of signaling cascades in ischemic RGCs that lead to their death.

视网膜缺血再灌注（IR）是多种眼部疾病（青光眼、糖尿病视网膜病变、缺血性视神经病变等）共有的病理机制，其最终结局为视网膜神经节细胞（RGC）死亡，进而引发视力损伤甚至失明。当前，我们调控视网膜IR发病机制的能力仍仅能大致延缓退行性病变的进展速率。研发能够阻断或逆转视网膜退行性变的新型治疗手段，有赖于对IR诱导RGC死亡相关分子机制的更深入阐释。本研究旨在明确缺血状态下RGC内导致其死亡的信号级联反应活性。