Evidence map›Paper›PMID 36982769›Full record

ArticleInternational journal of molecular sciences2023

Valproic Acid Inhibits Progressive Hereditary Hearing Loss in a KCNQ4 Variant Model through HDAC1 Suppression.

Yoon Seok Nam, Young Mi Choi, Sungsu Lee, Hyong-Ho Cho

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.6field-weighted citation impact, top 31% 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

4 citing papers in PubMed, 4 citations in OpenAlex.

  1. Review
  2. Hearing loss secondary to novel variants of the KCNQ4 gene.European archives of oto-rhino-laryngology : official journal of the European Federation of Oto-Rhino-Laryngological Societies (EUFOS) : affiliated with the German Society for Oto-Rhino-Laryngology - Head and Neck Surgery · 2025
    Observational
  3. Review
  4. Article
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

4 authors at 1 institution in 1 country.

Yoon Seok NamDepartment of Otolaryngology-Head and Neck Surgery, Chonnam National University Medical School and Chonnam National University Hospital, Gwangju 61469, Republic of Korea.ORCID 0000-0003-1432-3321
Young Mi ChoiDepartment of Otolaryngology-Head and Neck Surgery, Chonnam National University Medical School and Chonnam National University Hospital, Gwangju 61469, Republic of Korea.
Sungsu LeeDepartment of Otolaryngology-Head and Neck Surgery, Chonnam National University Medical School and Chonnam National University Hospital, Gwangju 61469, Republic of Korea.ORCID 0000-0002-0755-110X
Hyong-Ho ChoDepartment of Otolaryngology-Head and Neck Surgery, Chonnam National University Medical School and Chonnam National University Hospital, Gwangju 61469, Republic of Korea.ORCID 0000-0002-1331-4039
Chonnam National University Hospital · KR

Funding

Basic Science Research Program through the National Research Foundation of Korea, funded by the Ministry of Education, Science and Technology NRF-2020R1A2C1007473Chonnam National University 2019-0234Chonnam National University Hospital Biomedical Research Institute grant CRI18035-1Commercialization's Promotion Agency for R&D Outcomes (COMPA) grant funded by the Korean government (MSIT) No. 2022C100
6 · The paper itself

Abstract

Genetic or congenital hearing loss still has no definitive cure. Among genes related to genetic hearing loss, the potassium voltage-gated channel subfamily Q member 4 (KCNQ4) is known to play an essential role in maintaining ion homeostasis and regulating hair cell membrane potential. Variants of the KCNQ4 show reductions in the potassium channel activity and were responsible for non-syndromic progressive hearing loss. KCNQ4 has been known to possess a diverse variant. Among those variants, the KCNQ4 p.W276S variant produced greater hair cell loss related to an absence of potassium recycling. Valproic acid (VPA) is an important and commonly used histone deacetylase (HDAC) inhibitor for class I (HDAC1, 2, 3, and 8) and class IIa (HDAC4, 5, 7, and 9). In the current study, systemic injections of VPA attenuated hearing loss and protected the cochlear hair cells from cell death in the KCNQ4 p.W276S mouse model. VPA activated its known downstream target, the survival motor neuron gene, and increased acetylation of histone H4 in the cochlea, demonstrating that VPA treatment directly affects the cochlea. In addition, treatment with VPA increased the KCNQ4 binding with HSP90β by inhibiting HDAC1 activation in HEI-OC1 in an in vitro study. VPA is a candidate drug for inhibiting late-onset progressive hereditary hearing loss from the KCNQ4 p.W276S variant.

Indexed as

DeafnessHearing LossHearing Loss, SensorineuralAnimalsHair Cells, AuditoryHistone Deacetylase 1Histone Deacetylase InhibitorsKCNQ Potassium ChannelsMiceValproic AcidHdac1 protein, mouseHistone Deacetylase 1Histone Deacetylase InhibitorsKcnq4 protein, mouseKCNQ Potassium ChannelsValproic AcidHDAC1HDAC inhibitorhearing lossHSP90βKCNQ4valproic acid

Identifiers

PMID36982769
PMCPMC10058529
OpenAlexW4327736535

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.