September 2016
Volume 57, Issue 12
Open Access
ARVO Annual Meeting Abstract  |   September 2016
The role of transcellular mitophagy in glaucoma
Author Affiliations & Notes
  • Nicholas Marsh-Armstrong
    Johns Hopkins Univ Sch of Med, Baltimore, Maryland, United States
  • Footnotes
    Commercial Relationships   Nicholas Marsh-Armstrong, None
  • Footnotes
    Support  NIH Grant EY022680
Investigative Ophthalmology & Visual Science September 2016, Vol.57, No Pagination Specified. doi:
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      Nicholas Marsh-Armstrong; The role of transcellular mitophagy in glaucoma. Invest. Ophthalmol. Vis. Sci. 201657(12):.

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      © ARVO (1962-2015); The Authors (2016-present)

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Presentation Description : Mitochondria are essential organelles that perform many functions, including the production of the energy to drive biological processes within cells. Retinal ganglion cells have a unique dependence on their mitochondria, since mutations in both nuclear encoded and mitochondria encoded genes result in preferential loss of retinal ganglion cells. Mitophagy is the process by which damaged mitochondria are tagged and delivered to lysosomes for degradation, and until recently was believed to be a fully cell autonomous process. However, we recently discovered that large numbers of retinal ganglion cell mitochondria are shed from axons and degraded by phagocytic astrocytes at the optic nerve head of normal mice. These data will be presented along with recent data demonstrating that this process is regulated, including in animals that model discrete aspects of glaucoma. Since this unusual mode of mitochondria degradation occurs at the optic nerve head, the presumed site of axon damage in glaucoma, the possibility that transcellular mitophagy plays a role in glaucoma progression will be discussed.

This is an abstract that was submitted for the 2016 ARVO Annual Meeting, held in Seattle, Wash., May 1-5, 2016.


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