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The common hallmark of HONs, which in the large majority of cases are due to mitochondrial dysfunction as a common pathogenic mechanism, is the selective vulnerability and degeneration of retinal ganglion cells (RGCs) [1, 2, 6, 7]

Examining the pattern of change in these pathways at 4 and 8 h revealed the following patterns: two pathways remained upregulated (Lymphocyte Trafficking and Th2 Differentiation), three pathways reduced to the same level as control (Autophagy, Cell Adhesion, and Th1 Differentiation), and four were downregulated (Complement, Inflammasome, Type 1 IFN, and Type 2 IFN)

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Single-cell RNA-seq reveals the transcriptional landscape in ischemic stroke

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