Evidence map›Paper›PMID 39690754›Full record

ArticleBeijing da xue xue bao. Yi xue ban = Journal of Peking University. Health sciences2024

[Expression and significance of ferroptosis marker 4-HNE in

Kelin Zhao, Xue Xia, Naixu Shi, Han Zhou, Jingwen Gai, Ping Li

Abstract readEnglish Abstract
In one paragraph

Article in Beijing da xue xue bao. Yi xue ban = Journal of Peking University. Health sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Review
  2. 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

6 authors.

Kelin ZhaoDepartment of Rheumatology and Immunology, China-Japan Union Hospital, Jilin University, Changchun 130000, China.
Xue XiaDepartment of Rheumatology and Immunology, China-Japan Union Hospital, Jilin University, Changchun 130000, China.
Naixu ShiDepartment of Stomatology, China-Japan Union Hospital, Jilin University, Changchun 130000, China.
Han ZhouDepartment of Rheumatology and Immunology, China-Japan Union Hospital, Jilin University, Changchun 130000, China.
Jingwen GaiDepartment of Rheumatology and Immunology, China-Japan Union Hospital, Jilin University, Changchun 130000, China.
Ping LiDepartment of Rheumatology and Immunology, China-Japan Union Hospital, Jilin University, Changchun 130000, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveTo investigate the expression and physiological significance of the ferroptosis marker 4-hydroxynonenal (4-HNE) in myofibroblasts induced by transforming growth factor-β1 (TGF-β1), providing theoretical evidence for its potential role in the diagnosis and treatment of fibrosis in systemic sclerosis (SSc).

methodsMouse embryonic fibroblasts (NIH3t3) were cultured and divided into two groups after 12 h of starvation: the control group (cultured in 1% serum-containing medium) and the TGF-β1 group (cultured in 10 μg/L TGF-β1 with 1% serum-containing medium). Cell morphology changes in both groups were observed under a microscope. To confirm successful establishment of the SSc cell model, fibrosis markers were analyzed using reverse transcription quantitative real-time PCR (RT-qPCR) and Western blot. Next, flow cytometry was employed to assess the intracellular levels of reactive oxygen species (ROS) in both groups. Finally, Western blot and immunofluorescence staining were used to measure the expression of 4-HNE in the TGF-β1-treated cells.

resultsMicroscopic observations revealed that TGF-β1 treatment caused the NIH3t3 cells to transition from a typical spindle shape to a flat, polygonal shape with multiple protrusions, indicating fibroblast activation. The RT-qPCR and Western blot analyses showed that the expression of the fibrosis marker Vimentin was significantly upregulated in the TGF-β1 group compared with the control group (

conclusionTGF-β1 promotes fibroblast activation and fibrosis while inducing ROS production, leading to a marked increase in 4-HNE expression. Given the role of 4-HNE as a marker of lipid peroxidation and its elevated levels in the SSc cell model, this study suggests that 4-HNE could serve as a potential biomarker for fibrosis in SSc. The findings highlight the importance of investigating the mechanisms of 4-HNE in fibrosis and suggest that targeting this pathway could offer new therapeutic opportunities for treating SSc.

Indexed as

AldehydesFerroptosisReactive Oxygen SpeciesScleroderma, SystemicTransforming Growth Factor beta1AnimalsBiomarkersFibroblastsFibrosisMiceMyofibroblastsNIH 3T3 Cells4-hydroxy-2-nonenalAldehydesBiomarkersReactive Oxygen SpeciesTransforming Growth Factor beta1FerroptosisFibroblastsFibrosisSystemic sclerosis

Identifiers

PMID39690754
PMCPMC11652975

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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.