Evidence map›Paper›PMID 38877413›Full record

ArticleMolecular medicine (Cambridge, Mass.)2024

S100A6 Regulates nucleus pulposus cell apoptosis via Wnt/β-catenin signaling pathway: an in vitro and in vivo study.

Fengguang Yang, Yanni Duan, Yanhu Li, Daxue Zhu, Zhaoheng Wang, Zhangbin Luo, Yizhi Zhang, Guangzhi Zhang, Xuegang He, Xuewen Kang

Abstract read
In one paragraph

Article in Molecular medicine (Cambridge, Mass.), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
–field-weighted citation impact
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

8 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Pathogenic mechanisms of adult degenerative scoliosis.Frontiers in cell and developmental biology · 2026
    Review
  6. Article
  7. Review
  8. 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

10 authors.

Fengguang YangDepartment of Orthopedics, The Second Hospital of Lanzhou University, 82 Cuiying Men, Lanzhou, Gansu Province, 730030, China.
Yanni DuanDepartment of Orthopedics, The Second Hospital of Lanzhou University, 82 Cuiying Men, Lanzhou, Gansu Province, 730030, China.
Yanhu LiDepartment of Orthopedics, The Second Hospital of Lanzhou University, 82 Cuiying Men, Lanzhou, Gansu Province, 730030, China.
Daxue ZhuDepartment of Orthopedics, The Second Hospital of Lanzhou University, 82 Cuiying Men, Lanzhou, Gansu Province, 730030, China.
Zhaoheng WangDepartment of Orthopedics, The Second Hospital of Lanzhou University, 82 Cuiying Men, Lanzhou, Gansu Province, 730030, China.
Zhangbin LuoDepartment of Orthopedics, The Second Hospital of Lanzhou University, 82 Cuiying Men, Lanzhou, Gansu Province, 730030, China.
Yizhi ZhangDepartment of Orthopedics, The Second Hospital of Lanzhou University, 82 Cuiying Men, Lanzhou, Gansu Province, 730030, China.
Guangzhi ZhangDepartment of Orthopedics, The Second Hospital of Lanzhou University, 82 Cuiying Men, Lanzhou, Gansu Province, 730030, China.
Xuegang HeDepartment of Orthopedics, The Second Hospital of Lanzhou University, 82 Cuiying Men, Lanzhou, Gansu Province, 730030, China.
Xuewen KangDepartment of Orthopedics, The Second Hospital of Lanzhou University, 82 Cuiying Men, Lanzhou, Gansu Province, 730030, China. ery_kangxw@lzu.edu.cn.ORCID 0000-0002-5877-9198

Funding

Key R&D Plan of Gansu Provincial Department of Science and Technology-Social Development Projects, China 23YFFA0043National Natural Science Foundation of China 82272536
6 · The paper itself

Abstract

backgroundIntervertebral disc degeneration (IDD) is a common musculoskeletal degenerative disease, which often leads to low back pain and even disability, resulting in loss of labor ability and decreased quality of life. Although many progresses have been made in the current research, the underlying mechanism of IDD remains unclear. The apoptosis of nucleus pulposus (NP) cells (NPCs) is an important pathological mechanism in intervertebral disc degeneration (IDD). This study evaluated the relationship between S100A6 and NPCs and its underlying mechanism.

methodsMass spectrometry, bioinformatics, and quantitative real-time polymerase chain reaction (qRT-PCR) analyses were used to screen and verify hub genes for IDD in human IVD specimens with different degeneration degrees. Western blotting, immunohistochemistry (IHC), and/or immunofluorescence (IF) were used to detect the expression level of S100A6 in human NP tissues and NPCs. The apoptotic phenotype of NPCs and Wnt/β-catenin signaling pathway were evaluated using flow cytometry, western blotting, and IF. S100A6 was overexpressed or knocked down in NPCs to determine its impact on apoptosis and Wnt/β-catenin signaling pathway activity. Moreover, we used the XAV-939 to inhibit and SKL2001 to activate the Wnt/β-catenin signaling pathway. The therapeutic effect of S100A6 inhibition on IDD was also evaluated.

resultsS100A6 expression increased in IDD. In vitro, increased S100A6 expression promoted apoptosis in interleukin (IL)-1β-induced NPCs. In contrast, the inhibition of S100A6 expression partially alleviated the progression of annulus fibrosus (AF) puncture-induced IDD in rats. Mechanistic studies revealed that S100A6 regulates NPC apoptosis via Wnt/β-catenin signaling pathway.

conclusionsThis study showed that S100A6 expression increased during IDD and promoted NPCs apoptosis by regulating the Wnt/β-catenin signaling pathway, suggesting that S100A6 is a promising new therapeutic target for IDD.

Indexed as

ApoptosisIntervertebral Disc DegenerationNucleus PulposusS100 Calcium Binding Protein A6Wnt Signaling PathwayAdultAnimalsbeta CateninCell Cycle ProteinsDisease Models, AnimalFemaleHumansMaleMiddle AgedRatsRats, Sprague-Dawleybeta CateninCell Cycle ProteinsS100A6 protein, humanS100 Calcium Binding Protein A6ApoptosisIntervertebral disc degenerationS100A6Wnt/β-catenin signaling pathway

Identifiers

PMID38877413
PMCPMC11179208

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Registered trials

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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.