Evidence map›Paper›PMID 38093179›Full record

ArticleCellular & molecular biology letters2023

Molecular mechanism and therapeutic potential of HDAC9 in intervertebral disc degeneration.

Ming Lei, Hui Lin, Deyao Shi, Pan Hong, Hui Song, Bomansaan Herman, Zhiwei Liao, Cao Yang

Open access · goldAbstract read
In one paragraph

Article in Cellular & molecular biology letters, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
3.3field-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

12 citing papers in PubMed, 13 citations in OpenAlex.

  1. Research progress on lysine acetylation (Review).International journal of molecular medicine · 2026
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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

8 authors at 1 institution in 1 country.

Ming Lei *Department of Orthopedics, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, 1277 Jiefang Avenue, Wuhan, 430022, China. leiming2010@hust.edu.cn.ORCID http://orcid.org/0009-0004-3798-3335
Hui Lin *Department of Orthopedics, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, 1277 Jiefang Avenue, Wuhan, 430022, China.
Deyao Shi *Department of Orthopedics, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, 1277 Jiefang Avenue, Wuhan, 430022, China.
Pan HongDepartment of Orthopedics, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, 1277 Jiefang Avenue, Wuhan, 430022, China.
Hui SongDepartment of Orthopedics, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, 1277 Jiefang Avenue, Wuhan, 430022, China.
Bomansaan HermanDepartment of Orthopedics, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, 1277 Jiefang Avenue, Wuhan, 430022, China.
Zhiwei LiaoDepartment of Orthopedics, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, 1277 Jiefang Avenue, Wuhan, 430022, China. lzwhust@hust.edu.cn.
Cao YangDepartment of Orthopedics, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, 1277 Jiefang Avenue, Wuhan, 430022, China. caoyangunion@hust.edu.cn.
Union Hospital · CN

Funding

the Surface Project of Technical Innovation Special Project of Hubei Province 2021CFB591
6 · The paper itself

Abstract

backgroundIntervertebral disc degeneration (IVDD) is the major cause of low-back pain. Histone deacetylase 9 (HDAC9) was dramatically decreased in the degenerative nucleus pulposus (NP) samples of patients with intervertebral disc degeneration (IVDD) according to bioinformatics analysis of Gene Expression Omnibus (GEO) GSE56081 dataset. This study aims to investigate the role of HDAC9 in IVDD progression.

methodsThe contribution of HDAC9 to the progression of IVDD was assessed using HDAC9 knockout (HDAC9

resultsHDAC9 was statistically decreased in the NP tissues in aged mice. HDAC9

conclusionOur results suggest that HDAC9 plays an important role in the development and progression of IVDD. It might be required to protect NP cells against the loss of cell viability and apoptosis by inhibiting RUNX3 acetylation and expression during IVDD. Together, our findings suggest that HDAC9 may be a potential therapeutic target in IVDD.

Indexed as

Intervertebral Disc DegenerationNucleus PulposusAnimalsApoptosisHistone DeacetylasesHumansMiceRepressor ProteinsRNA, MessengerSignal TransductionHDAC9 protein, humanHdac9 protein, mouseHistone DeacetylasesRepressor ProteinsRNA, MessengerApoptosisCell viabilityHDAC9Intervertebral disc degenerationRUNX3

Identifiers

PMID38093179
PMCPMC10717711
OpenAlexW4389685142

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.