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@ARTICLE{Bell:151653,
      author       = {Bell, Katharina and Rosignol, Ines and Sierra-Filardi,
                      Elena and Rodriguez-Muela, Natalia and Schmelter, Carsten
                      and Cecconi, Francesco and Grus, Franz and Boya, Patricia},
      title        = {{A}ge related retinal {G}anglion cell susceptibility in
                      context of autophagy deficiency},
      journal      = {Cell death discovery},
      volume       = {6},
      number       = {1},
      issn         = {2058-7716},
      address      = {London},
      publisher    = {Nature Publishing Group306324},
      reportid     = {DZNE-2020-01232},
      pages        = {21},
      year         = {2020},
      abstract     = {Glaucoma is a common age-related disease leading to
                      progressive retinal ganglion cell (RGC) death, visual field
                      defects and vision loss and is the second leading cause of
                      blindness in the elderly worldwide. Mitochondrial
                      dysfunction and impaired autophagy have been linked to
                      glaucoma and induction of autophagy shows neuroprotective
                      effects in glaucoma animal models. We have shown that
                      autophagy decreases with aging in the retina and that
                      autophagy can be neuroprotective for RGCs, but it is
                      currently unknown how aging and autophagy deficiency impact
                      RGCs susceptibility and survival. Using the optic nerve
                      crush model in young and olWelcome@1234d Ambra1+/gt
                      (autophagy/beclin-1 regulator 1+/gt) mice we analysed the
                      contribution of autophagy deficiency on retinal ganglion
                      cell survival in an age dependent context. Interestingly,
                      old Ambra1+/gt mice showed decreased RGC survival after
                      optic nerve crush in comparison to old Ambra1+/+, an effect
                      that was not observed in the young animals. Proteomics and
                      mRNA expression data point towards altered oxidative stress
                      response and mitochondrial alterations in old Ambra1+/gt
                      animals. This effect is intensified after RGC axonal damage,
                      resulting in reduced oxidative stress response showing
                      decreased levels of Nqo1, as well as failure of Nrf2
                      induction in the old Ambra1+/gt. Old Ambra1+/gt also failed
                      to show increase in Bnip3l and Bnip3 expression after optic
                      nerve crush, a response that is found in the Ambra1+/+
                      controls. Primary RGCs derived from Ambra1+/gt mice show
                      decreased neurite projection and increased levels of
                      apoptosis in comparison to Ambra1+/+ animals. Our results
                      lead to the conclusion that oxidative stress response
                      pathways are altered in old Ambra1+/gt mice leading to
                      impaired damage responses upon additional external stress
                      factors.},
      cin          = {AG Rodriguez-Muela},
      ddc          = {610},
      cid          = {I:(DE-2719)1713001},
      pnm          = {344 - Clinical and Health Care Research (POF3-344)},
      pid          = {G:(DE-HGF)POF3-344},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:32337073},
      pmc          = {pmc:PMC7165178},
      doi          = {10.1038/s41420-020-0257-4},
      url          = {https://pub.dzne.de/record/151653},
}