Evidence map›Paper›PMID 38802345›Full record

ArticleInternational journal of oral science2024

A multi-platform analysis of human gingival crevicular fluid reveals ferroptosis as a relevant regulated cell death mechanism during the clinical progression of periodontitis.

Alfredo Torres, M Angélica Michea, Ákos Végvári, Marion Arce, Valentina Pérez, Marcela Alcota, Alicia Morales, Rolando Vernal, Mauricio Budini, Roman A Zubarev and 1 more

Abstract read
In one paragraph

Article in International journal of oral science, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing 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

16 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

11 authors.

Alfredo TorresLaboratory of Experimental Immunology & Cancer, Faculty of Dentistry, University of Chile, Santiago, Chile.ORCID 0000-0002-7593-6829
M Angélica MicheaDepartment of Conservative Dentistry, Faculty of Dentistry, University of Chile, Santiago, Chile.
Ákos VégváriDivision of Chemistry I, Department of Medical Biochemistry and Biophysics, Karolinska Institutet, Stockholm, Sweden.ORCID 0000-0002-1287-0906
Marion ArceDepartment of Conservative Dentistry, Faculty of Dentistry, University of Chile, Santiago, Chile.
Valentina PérezLaboratory of Experimental Immunology & Cancer, Faculty of Dentistry, University of Chile, Santiago, Chile.
Marcela AlcotaDepartment of Conservative Dentistry, Faculty of Dentistry, University of Chile, Santiago, Chile.
Alicia MoralesDepartment of Conservative Dentistry, Faculty of Dentistry, University of Chile, Santiago, Chile.
Rolando VernalDepartment of Conservative Dentistry, Faculty of Dentistry, University of Chile, Santiago, Chile.ORCID 0000-0002-1391-320X
Mauricio BudiniLaboratory of Cellular and Molecular Pathology, Institute for Research in Dental Sciences, Faculty of Dentistry, University of Chile, Santiago, Chile.
Roman A ZubarevDivision of Chemistry I, Department of Medical Biochemistry and Biophysics, Karolinska Institutet, Stockholm, Sweden.
Fermín E GonzálezLaboratory of Experimental Immunology & Cancer, Faculty of Dentistry, University of Chile, Santiago, Chile. fgonzalez@uchile.cl.

Funding

Fondo Nacional de Desarrollo Científico y Tecnológico (National Fund for Scientific and Technological Development) 1220999Universidad de Chile (University of Chile) FIOUCH 23-02
6 · The paper itself

Abstract

Ferroptosis is implicated in the pathogenesis of numerous chronic-inflammatory diseases, yet its association with progressive periodontitis remains unexplored. To investigate the involvement and significance of ferroptosis in periodontitis progression, we assessed sixteen periodontitis-diagnosed patients. Disease progression was clinically monitored over twelve weeks via weekly clinical evaluations and gingival crevicular fluid (GCF) collection was performed for further analyses. Clinical metrics, proteomic data, in silico methods, and bioinformatics tools were combined to identify protein profiles linked to periodontitis progression and to explore their potential connection with ferroptosis. Subsequent western blot analyses validated key findings. Finally, a single-cell RNA sequencing (scRNA-seq) dataset (GSE164241) for gingival tissues was analyzed to elucidate cellular dynamics during periodontitis progression. Periodontitis progression was identified as occurring at a faster rate than traditionally thought. GCF samples from progressing and non-progressing periodontal sites showed quantitative and qualitatively distinct proteomic profiles. In addition, specific biological processes and molecular functions during progressive periodontitis were revealed and a set of hub proteins, including SNCA, CA1, HBB, SLC4A1, and ANK1 was strongly associated with the clinical progression status of periodontitis. Moreover, we found specific proteins - drivers or suppressors - associated with ferroptosis (SNCA, FTH1, HSPB1, CD44, and GCLC), revealing the co-occurrence of this specific type of regulated cell death during the clinical progression of periodontitis. Additionally, the integration of quantitative proteomic data with scRNA-seq analysis suggested the susceptibility of fibroblasts to ferroptosis. Our analyses reveal proteins and processes linked to ferroptosis for the first time in periodontal patients, which offer new insights into the molecular mechanisms of progressive periodontal disease. These findings may lead to novel diagnostic and therapeutic strategies.

Indexed as

Disease ProgressionFerroptosisGingival Crevicular FluidPeriodontitisAdultBlotting, WesternCell DeathFemaleHumansMaleMiddle AgedProteomics

Identifiers

PMID38802345
PMCPMC11130186

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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.