<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Ihadadene K</submitter><funding>DAAD Stipend for International Students</funding><funding>Charlotte and Tistou Kerstan Foundation</funding><funding>Zinke Heritage foundation</funding><funding>ProRetina Germany Foundation</funding><funding>German Ministry for Education and Research (BMBF)</funding><funding>INTHERAPI Graduate School and a Stipend From the Erasmus+ Programme of the European Union</funding><pagination>e70072</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC12019586</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>169(4)</volume><pubmed_abstract>The axons of retinal ganglion cells (RGCs) form the optic nerve, which relays visual information to the brain. RGC degeneration is the root cause of a variety of blinding diseases linked to optic nerve damage, including glaucoma, the second leading cause of blindness worldwide. The underlying cellular mechanisms of RGC degeneration are largely unclear; yet, they have been connected to excessive production of the signalling molecule nitric oxide (NO) by nitric oxide synthase (NOS). NO activates soluble guanylate cyclase (sGC), which subsequently produces the second messenger cyclic guanosine monophosphate (cGMP). This, in turn, activates protein kinase G (PKG), which can phosphorylate downstream protein targets. To study the role of NO/cGMP/PKG signalling in RGC degeneration, we used organo</pubmed_abstract><journal>Journal of neurochemistry</journal><pubmed_title>Inhibition of cGMP-Signalling Rescues Retinal Ganglion Cells From Axotomy-Induced Degeneration.</pubmed_title><pmcid>PMC12019586</pmcid><funding_grant_id>16GW0267K</funding_grant_id><pubmed_authors>Paquet-Durand F</pubmed_authors><pubmed_authors>Zhu Y</pubmed_authors><pubmed_authors>Ihadadene K</pubmed_authors><pubmed_authors>Fallatah AHA</pubmed_authors><pubmed_authors>Tolone A</pubmed_authors></additional><is_claimable>false</is_claimable><name>Inhibition of cGMP-Signalling Rescues Retinal Ganglion Cells From Axotomy-Induced Degeneration.</name><description>The axons of retinal ganglion cells (RGCs) form the optic nerve, which relays visual information to the brain. RGC degeneration is the root cause of a variety of blinding diseases linked to optic nerve damage, including glaucoma, the second leading cause of blindness worldwide. The underlying cellular mechanisms of RGC degeneration are largely unclear; yet, they have been connected to excessive production of the signalling molecule nitric oxide (NO) by nitric oxide synthase (NOS). NO activates soluble guanylate cyclase (sGC), which subsequently produces the second messenger cyclic guanosine monophosphate (cGMP). This, in turn, activates protein kinase G (PKG), which can phosphorylate downstream protein targets. To study the role of NO/cGMP/PKG signalling in RGC degeneration, we used organo</description><dates><release>2025-01-01T00:00:00Z</release><publication>2025 Apr</publication><modification>2026-06-02T18:24:44.16Z</modification><creation>2025-07-01T03:05:33.698Z</creation></dates><accession>S-EPMC12019586</accession><cross_references><pubmed>40270249</pubmed><doi>10.1111/jnc.70072</doi></cross_references></HashMap>