Evidence map›Paper›PMID 37597101›Full record

ArticleClinical rheumatology2023

Demethylation of CDKN2A in systemic lupus erythematosus and rheumatoid arthritis: a blood biomarker for diagnosis and assessment of disease activity.

Abdollah Gravand, Samira Alesaeidi, Shahrouz Khoshbakht, Mozhdeh Saghaei, Taiebe Kenarangi, Meysam Mosallaei, Mohsen Soosanabadi

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Article in Clinical rheumatology, 2023. 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
2.2field-weighted citation impact, top 12% 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

8 citing papers in PubMed, 9 citations in OpenAlex.

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  8. Promoter Methylation ofAdvanced biomedical research · 2025
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4 · The record

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5 · Who and what money

Authors and funding

7 authors at 5 institutions in 1 country.

Abdollah GravandDepartment of Genetics, Faculty of Sciences, Shahid Chamran University of Ahvaz, Ahvaz, Iran.
Samira AlesaeidiDepartment of Internal Medicine and Rheumatology, Rheumatology Research Center, Tehran University of Medical Sciences, Tehran, Iran.
Shahrouz KhoshbakhtStudent Research Committee, University of Social Welfare and Rehabilitation Science, Tehran, Iran.
Mozhdeh SaghaeiDepartment of Internal Medicine, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran.
Taiebe KenarangiStudent Research Committee, Faculty of Statistics, University of Social Welfare and Rehabilitation Science, Tehran, Iran.
Meysam MosallaeiPersonalized Medicine and Genometabolomics Research Center, Hope Generation Foundation, Tehran, Iran.
Mohsen SoosanabadiDepartment of Medical Genetics, Semnan University of Medical Sciences, Semnan, Iran. m_soosanabadi@yahoo.com.ORCID http://orcid.org/0000-0003-0186-9464
University of Social Welfare and Rehabilitation Sciences · IRIsfahan University of Medical Sciences · IRSemnan University of Medical Sciences · IRShahid Chamran University of Ahvaz · IRTehran University of Medical Sciences · IR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

INTRODUCTION/

objectivesConsidering the phenotypic and serological heterogeneity of systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA), significant challenges may intervene with the precise diagnosis. In this regard, numerous studies have shown that changes in DNA methylation levels can be used to distinguish between healthy individuals and those with SLE and RA, as well as to predict disease activity and prognosis.

methodsIn the current study, we evaluated quantitative methylation level of CDKN2A promoter in peripheral blood mononuclear cells (PBMCs) of SLE and RA patients, and healthy controls by methylation-quantification of endonuclease-resistant DNA (MethyQESD), a bisulfite conversion-independent method.

resultsOur findings revealed an excessive hypomethylation of CDKN2A in SLE and RA patients compared to healthy individuals (P < 0.001). Besides, by determining efficient cutoff value, the specificity of CDKN2A for correct diagnosis of healthy subjects was measured to be 77.30% and the sensitivity for SLE and RA diagnosis were 81.33%, and 72%, respectively. Furthermore, CDKN2A methylation level was shown to be positively associated with C3 and C4 levels and negatively associated with anti‑dsDNA concentration (P < 0.001). Moreover, a statistically significant difference in the DNA methylation levels of CDKN2A promoter was identified between SLE cases with age of ≤ 18 and patients with > 18 years of age (P = 0.025).

conclusionOur findings demonstrated that CDKN2A methylation levels in PBMCs of SLE and RA patients could be used as a promising diagnostic biomarker. The significant association between hypomethylation of CDKN2A promoter and disease activity factors in SLE patients, is suggesting that CDKN2A hypomethylation could be used as an alternative biomarker for assessment of disease activity. Key Points • Several studies have reported increased expression of CDKN2A in SLE and RA suggesting that it may be involved in the pathogenesis of these disorders. • CDKN2A hypomethylation has been implicated in different autoimmune diseases. • Our findings demonstrated that CDKN2A methylation levels in PBMCs of SLE and RA patients could be used as a promising diagnostic and prognostic biomarker.

Indexed as

Arthritis, RheumatoidLupus Erythematosus, SystemicAdolescentBiomarkersCyclin-Dependent Kinase Inhibitor p16DemethylationHumansLeukocytes, MononuclearBiomarkersCDKN2A protein, humanCyclin-Dependent Kinase Inhibitor p16BiomarkerCDKN2AMethylationRheumatoid arthritisSystemic lupus erythematosus

Identifiers

PMID37597101
OpenAlexW4386001412

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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.