Evidence map›Paper›PMID 34733937›Full record

ArticleAnnals of translational medicine2021

Transcription factor EB mediates oxidative stress-induced intervertebral disc degeneration via the NF-κB signaling pathway.

He Liang, Zhou Liu, Yunhao Wang, Deguo Wang, Jiwei Tian

Open access · diamondAbstract read
In one paragraph

Article in Annals of translational medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.9field-weighted citation impact, top 26% 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

5 citing papers in PubMed, 7 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. The Effect ofOxidative medicine and cellular longevity · 2022
    Article
  5. Review
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 4 institutions in 1 country.

He LiangClinical Medical College, Shanghai General Hospital of Nanjing Medical University, Shanghai, China.
Zhou LiuDepartment of Orthopedics, Fuyang Fifth People's Hospital, Fuyang, China.
Yunhao WangDepartment of Spinal Surgery, Changzheng Hospital Affiliated to Second Military Medical University, Shanghai, China.
Deguo WangDepartment of Orthopedics, Shanghai Songjiang District Central Hospital, Shanghai, China.
Jiwei TianDepartment of Orthopedics, Shanghai General Hospital of Nanjing Medical University, Shanghai, China.
Second Military Medical University · CNShanghai First People's Hospital · CNShanghai Medical College of Fudan University · CNSongjiang District Central Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundIt is well known that the intervertebral disc is aggravated by a significant increase in the number of senescent cells, and oxidative stress (OS) is related to the deterioration of this tissue. Transcription factor EB (TFEB) can protect cells from OS. Accordingly, we investigated whether TFEB can prevent OS in human nucleus pulposus (NP) cells.

methodsFirst, TFEB expression was investigated in human NP tissue samples with different degrees of degeneration. NP cells were treated with different concentrations of hydrogen peroxide (H

resultsWe found that the expression of TFEB decreased stepwise as the degree of intervertebral disc degeneration (IDD) increased. When the NP cells were treated with H

conclusionsThis study suggests that OS is associated with the development of IDD. TFEB mediates OS-induced IDD via the NF-κB signaling pathway. The

Indexed as

intervertebral disc degeneration (IDD)Oxidative stress (OS)transcription factor EB (TFEB)

Identifiers

PMID34733937
PMCPMC8506563
OpenAlexW3201513801

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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 Socratic graph.