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. 2012 May 4;53(5):2476-81.
doi: 10.1167/iovs.12-9483h.

The cell and molecular biology of glaucoma: mechanisms of retinal ganglion cell death

Robert W Nickells  1
Affiliations

The cell and molecular biology of glaucoma: mechanisms of retinal ganglion cell death

Robert W Nickells. Invest Ophthalmol Vis Sci. .
No abstract available

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Figures

Figure 1.
Figure 1.
A hypothetical timeline of molecular events activated in retinal ganglion cells after axonal damage. The events precipitated by BAX activation (yellow background) center on dysfunction of the mitochondria and represent a point at which rescue of the cell is not possible. Early activation events (teal background) include the activation of several kinases including p38, JNK2/3, and JUN, as well as cell atrophy leading to shrinkage and the recruitment of some members of the BH3-only peptide family, which likely facilitate BAX activation. Later events are likely to include caspase activation and possibly endoplasmic reticulum (ER) stress, but the ordering of this latter event is not conclusive. Once some ganglion cells begin to die, it is also possible that secondary degenerative events are set in motion, which include the activation of both macro- and microglia and the production of the inflammatory cytokine TNFα (light blue background). TNFα may result in the death of adjacent unaffected ganglion cells or may exacerbate the death of affected cells by amplifying their level of damage and BAX activation.
See this image and copyright information in PMC

References

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