<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Zhu Y</submitter><funding>NEI NIH HHS</funding><pagination>60</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC12721432</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>66(15)</volume><pubmed_abstract>&lt;h4>Purpose&lt;/h4>As the sole retinal output neurons, retinal ganglion cells (RGCs) transmit all visual information from the retina to the brain. RGCs do not regenerate, and effective therapies for promoting RGC survival and axon regeneration in glaucoma and other optic neuropathies comprise an unmet clinical need. Histone deacetylases (HDACs) are epigenetic modifiers that repress gene transcription. Here, we identify a role for HDAC4 in RGC neurodegeneration and axon regeneration.&lt;h4>Methods&lt;/h4>The role of HDAC4 in RGC neuroprotection and axon regeneration was studied in the mouse optic nerve crush (ONC) model for optic neuropathy by RGC transduction in vivo with adeno-associated virus vectors. RGC gene expression in vivo was studied by single cell RNA sequencing (scRNA-seq).&lt;h4>Results&lt;/h</pubmed_abstract><journal>Investigative ophthalmology &amp; visual science</journal><pubmed_title>HDAC4 Promotes Neuroprotection of Retinal Ganglion Cells After Optic Nerve Injury.</pubmed_title><pmcid>PMC12721432</pmcid><funding_grant_id>R01 EY032416</funding_grant_id><funding_grant_id>R01 EY036028</funding_grant_id><funding_grant_id>R01 EY031167</funding_grant_id><funding_grant_id>P30 EY026877</funding_grant_id><pubmed_authors>Nair RV</pubmed_authors><pubmed_authors>Xia X</pubmed_authors><pubmed_authors>Goldberg JL</pubmed_authors><pubmed_authors>Li J</pubmed_authors><pubmed_authors>Russano K</pubmed_authors><pubmed_authors>Huie EL</pubmed_authors><pubmed_authors>Chang HV</pubmed_authors><pubmed_authors>Kapiloff MS</pubmed_authors><pubmed_authors>Ochoa JR</pubmed_authors><pubmed_authors>Zhu Y</pubmed_authors><pubmed_authors>Luo Z</pubmed_authors><pubmed_authors>Yan W</pubmed_authors><pubmed_authors>Nahmou M</pubmed_authors><pubmed_authors>Li X</pubmed_authors><pubmed_authors>Bian M</pubmed_authors><pubmed_authors>Thakur HS</pubmed_authors><pubmed_authors>Sun CB</pubmed_authors></additional><is_claimable>false</is_claimable><name>HDAC4 Promotes Neuroprotection of Retinal Ganglion Cells After Optic Nerve Injury.</name><description>&lt;h4>Purpose&lt;/h4>As the sole retinal output neurons, retinal ganglion cells (RGCs) transmit all visual information from the retina to the brain. RGCs do not regenerate, and effective therapies for promoting RGC survival and axon regeneration in glaucoma and other optic neuropathies comprise an unmet clinical need. Histone deacetylases (HDACs) are epigenetic modifiers that repress gene transcription. Here, we identify a role for HDAC4 in RGC neurodegeneration and axon regeneration.&lt;h4>Methods&lt;/h4>The role of HDAC4 in RGC neuroprotection and axon regeneration was studied in the mouse optic nerve crush (ONC) model for optic neuropathy by RGC transduction in vivo with adeno-associated virus vectors. RGC gene expression in vivo was studied by single cell RNA sequencing (scRNA-seq).&lt;h4>Results&lt;/h</description><dates><release>2025-01-01T00:00:00Z</release><publication>2025 Dec</publication><modification>2026-06-06T16:04:03.994Z</modification><creation>2026-06-02T03:11:47.666Z</creation></dates><accession>S-EPMC12721432</accession><cross_references><pubmed>41533933</pubmed><doi>10.1167/iovs.66.15.60</doi></cross_references></HashMap>