Evidence map›Paper›PMID 30910408›Full record

ArticleExperimental neurology2019

HDAC5 promotes optic nerve regeneration by activating the mTOR pathway.

Wolfgang Pita-Thomas, Marcus Mahar, Avni Joshi, Di Gan, Valeria Cavalli

Open access · greenAbstract read
In one paragraph

Article in Experimental neurology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
3.2field-weighted citation impact, top 8% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

29 citing papers in PubMed, 49 citations in OpenAlex.

  1. Review
  2. Article
  3. Translational control of innate barrier defense by the gut microbiota.bioRxiv : the preprint server for biology · 2025
    Article
  4. Genes in Axonal Regeneration.Molecular neurobiology · 2024
    Review
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 1 institution in 1 country.

Wolfgang Pita-ThomasDepartment of Neuroscience, Washington University School of Medicine, St. Louis, MO 63110, United States of America.
Marcus MaharDepartment of Neuroscience, Washington University School of Medicine, St. Louis, MO 63110, United States of America.
Avni JoshiDepartment of Neuroscience, Washington University School of Medicine, St. Louis, MO 63110, United States of America.
Di GanDepartment of Neuroscience, Washington University School of Medicine, St. Louis, MO 63110, United States of America; Department of Neuroscience, Brandeis University, Waltham, MA 02453, United States of America.
Valeria CavalliDepartment of Neuroscience, Washington University School of Medicine, St. Louis, MO 63110, United States of America; Center of Regenerative Medicine, Washington University School of Medicine, St. Louis, MO 63110, United States of America; Hope Center for Neurological Disorders, Washington University School of Medicine, St. Louis, MO 63110, United States of America. Electronic address: cavalli@wustl.edu.
Washington University in St. Louis · US

Funding

MECHANISMS OF CHROMATIN REMODELING PROMOTING AXON REGENERATIONR01NS096034 · NINDS · WASHINGTON UNIVERSITY · PI CAVALLI, VALERIA · 2016 to 2020
$1.7M
MICROTUBULE POST-TRANSLATIONAL MODIFICATIONS IN AXON REGENERATIONR01NS082446 · NINDS · WASHINGTON UNIVERSITY · PI CAVALLI, VALERIA · 2013 to 2017
$1.7M
IDENTIFYING EPIGENETIC MODIFIERS PROMOTING OPTIC NERVE REGENERATIONR21EY029077 · NEI · WASHINGTON UNIVERSITY · PI CAVALLI, VALERIA · 2018 to 2019
$419k
NEI NIH HHS R21 EY029077NINDS NIH HHS R01 NS082446NINDS NIH HHS R01 NS096034
6 · The paper itself

Abstract

Neurons in the central nervous system (CNS) regenerate poorly compared to their counterparts in the peripheral nervous system. We previously showed that, in peripheral sensory neurons, nuclear HDAC5 inhibits the expression of regenerative associated genes. After nerve injury, HDAC5 is exported to the cytoplasm to promote axon regeneration. Here we investigated the role of HDAC5 in retinal ganglion cells (RGCs), a CNS neuron which fails to survive and regenerate axons after injury. In contrast to PNS neurons, we found that HDAC5 is mostly cytoplasmic in naïve RGCs and its localization is not affected by optic nerve injury, suggesting that HDAC5 does not directly suppress regenerative associated genes in these cells. Manipulation of the PKCμ pathway, the canonical pathway that regulates HDAC5 localization in PNS neurons by phosphorylating serine 259 and 498, and other pathways that regulate nuclear/cytoplasmic transport, did not affect HDAC5 cytoplasmic localization in RGC. Also, an HDAC5 mutant whose serine 259 and 488 were replaced by alanine (HDAC5

Indexed as

AnimalsHistone DeacetylasesMiceMice, Inbred C57BLNerve RegenerationOptic NerveOptic Nerve InjuriesRatsRats, Sprague-DawleyRetinal Ganglion CellsSignal TransductionTOR Serine-Threonine KinasesHistone DeacetylasesTOR Serine-Threonine KinasesHDAC5mTOROptic nerve regenerationRetinal ganglion cellsZymosan

Identifiers

PMID30910408
PMCPMC6544474
OpenAlexW2923047730

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.