Evidence map›Paper›PMID 39752341›Full record

ArticlePloS one2025

MARCHF8-mediated ubiquitination via TGFBI regulates NF-κB dependent inflammatory responses and ECM degradation in intervertebral disc degeneration.

Xingpeng Zhang, Guang Li, Fang Tan, Tao Yu, Chengping Xu, Kai Li, Feng Zhang, Meiyan Zhang, Jian Wang

Abstract read
In one paragraph

Article in PloS one, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing 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

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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

6 citing papers in PubMed.

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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

9 authors.

Xingpeng ZhangDepartment of Orthopedics, Shanghai Pudong New Area People's Hospital, Shanghai, China.
Guang LiDepartment of Traumatic Surgery, Emergency Center, Shanghai East Hospital, Tongji University School of Medicine, Shanghai, China.
Fang TanDepartment of Orthopedics, Shanghai Pudong New Area People's Hospital, Shanghai, China.
Tao YuDepartment of Orthopedics, Shanghai Pudong New Area People's Hospital, Shanghai, China.
Chengping XuDepartment of Orthopedics, Shanghai Pudong New Area People's Hospital, Shanghai, China.
Kai LiDepartment of Orthopedics, Shanghai Pudong New Area People's Hospital, Shanghai, China.
Feng ZhangDepartment of Orthopedics, Shanghai Pudong New Area People's Hospital, Shanghai, China.
Meiyan ZhangShanghai Circle Harmony Xinyong Clinic, Shanghai, China.
Jian WangDepartment of Orthopedics, Shanghai Pudong New Area People's Hospital, Shanghai, China.ORCID 0009-0007-1268-113X

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimTo explore the role of the hub gene Transforming Growth Factor Beta Induced (TGFBI) in Intervertebral disc degeneration (IDD) pathogenesis and its regulatory relationship with Membrane Associated Ring-CH-Type Finger 8 (MARCHF8).

backgroundIDD is a prevalent musculoskeletal disorder leading to spinal pathology. Despite its ubiquity and impact, effective therapeutic strategies remain to be explored.

objectiveIdentify key modules associated with IDD and understand the impact of TGFBI on nucleus pulposus (NP) cell behavior, extracellular matrix (ECM)-related proteins, and the Nuclear Factor kappa-light-chain-enhancer of Activated B cells (NF-κB) signaling pathway.

methodsThe GSE146904 dataset underwent Weighted Gene Co-Expression Network Analysis (WGCNA) for key module identification and Differentially Expressed Genes (DEGs) screening. Intersection analysis, network analysis, and co-expression identified TGFBI as a hub gene. In vitro experiments delved into the interplay between TGFBI and MARCHF8 and their effects on NP cells.

resultsWGCNA linked the MEturquoise module with IDD samples, revealing 145 shared genes among DEGs. In vitro findings indicated that MARCHF8 determines TGFBI expression. TGFBI boosts apoptosis and ECM breakdown in Lipopolysaccharide-stimulated (LPS-stimulated) NP cells. Altering TGFBI levels modulated these effects and the NF-κB signaling pathway, influencing inflammatory cytokine concentrations. Moreover, MARCHF8 ubiquitination controlled TGFBI expression.

conclusionTGFBI, modulated by MARCHF8, significantly influences IDD progression by affecting NP cell apoptosis, ECM degradation, and inflammation through the NF-κB signaling pathway.

Indexed as

Extracellular MatrixIntervertebral Disc DegenerationNF-kappa BNucleus PulposusSignal TransductionUbiquitinationAnimalsExtracellular Matrix ProteinsHumansInflammationTransforming Growth Factor betaUbiquitin-Protein LigasesExtracellular Matrix ProteinsNF-kappa BTransforming Growth Factor betaUbiquitin-Protein Ligases

Identifiers

PMID39752341
PMCPMC11698339

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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.