Evidence map›Paper›PMID 32936764›Full record

ArticleJournal of clinical research in pediatric endocrinology2021

Transforming Growth Factor-β1 and Receptor for Advanced Glycation End Products Gene Expression and Protein Levels in Adolescents with Type 1 iabetes Mellitus

Ana Ninić, Dragana Bojanin, Miron Sopić, Marija Mihajlović, Jelena Munjas, Tatjana Milenković, Aleksandra Stefanović, Jelena Vekić, Vesna Spasojević-Kalimanovska

Open access · goldAbstract read
In one paragraph

Article in Journal of clinical research in pediatric endocrinology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.5field-weighted citation impact, top 36% 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

4 citing papers in PubMed, 8 citations in OpenAlex.

  1. Article
  2. Narra J · 2025
    Article
  3. Article
  4. 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

9 authors at 2 institutions in 1 country.

Ana NinićUniversity of Belgrade Faculty of Pharmacy, Department for Medical Biochemistry, Belgrade, SerbiaORCID 0000-0003-3838-1606
Dragana BojaninMother and Child Health Care Institute of Serbia “Dr Vukan Čupić”, Biochemical Laboratory, Belgrade, SerbiaORCID 0000-0002-8382-822X
Miron SopićUniversity of Belgrade Faculty of Pharmacy, Department for Medical Biochemistry, Belgrade, SerbiaORCID 0000-0003-3283-9487
Marija MihajlovićUniversity of Belgrade Faculty of Pharmacy, Department for Medical Biochemistry, Belgrade, SerbiaORCID 0000-0003-3307-0809
Jelena MunjasUniversity of Belgrade Faculty of Pharmacy, Department for Medical Biochemistry, Belgrade, SerbiaORCID 0000-0002-4576-1722
Tatjana MilenkovićMother and Child Health Care Institute of Serbia “Dr Vukan Čupić”, Department of Endocrinology, Belgrade, SerbiaORCID 0000-0002-5239-7113
Aleksandra StefanovićUniversity of Belgrade Faculty of Pharmacy, Department for Medical Biochemistry, Belgrade, SerbiaORCID 0000-0002-0331-6807
Jelena VekićUniversity of Belgrade Faculty of Pharmacy, Department for Medical Biochemistry, Belgrade, SerbiaORCID 0000-0001-7445-0504
Vesna Spasojević-KalimanovskaUniversity of Belgrade Faculty of Pharmacy, Department for Medical Biochemistry, Belgrade, SerbiaORCID 0000-0003-1617-7559
University of Belgrade · RSInstitute of Public Health of Serbia · RS

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Objective: Type 1 diabetes (T1D) mellitus is one of the most frequent autoimmune diseases in childhood. Chronic complications are the main causes of cardiovascular morbidity and mortality in T1D. Although interactions between advanced glycation end products (AGE) and their receptors (RAGE) and transforming growth factor-β1 (TGF-β1) are implicated in development and progression of diabetic microand macro-vascular complications, they also have important roles in immune system regulation. Methods: Blood samples were obtained from 156 adolescents with T1D and 80 apparently healthy controls. T1D patients diagnosed with any other autoimmune disease and receiving any kind of drugs except insulin therapy were excluded from this study. Exclusion criteria for controls were positive family history of T1D and drugs/supplements application. TGF-β1 and transmembrane full-length RAGE (flRAGE) messenger ribonucleic acid (mRNA) levels in peripheral blood mononuclear cells (PBMC) were obtained by quantitative polymerase chain reaction (qPCR) method. Circulating levels of biochemical markers, TGF-β1 and soluble RAGE (sRAGE) levels were also determined. Results: TGF-β1 and flRAGE mRNA levels were significantly higher in controls compared to patients (p<0.001, for both). However, TGF-β1 and sRAGE levels were higher in patients than controls (p<0.001, for both). There were significant independent associations of all mRNA and protein levels with T1D. TGF-β1 mRNA was the only marker independently negatively associated with urinary albumin excretion rate in T1D adolescents (p=0.005). Conclusion: Our results indicated gene expression downregulation of TGF-β1 and flRAGE in PBMC of T1D adolescents. TGF-β1 mRNA downregulation may be useful for predicting early elevation of urinary albumin excretion rate.

Indexed as

AdolescentChildDiabetes Mellitus, Type 1Down-RegulationFemaleHumansMaleReceptor for Advanced Glycation End ProductsTransforming Growth Factor beta1AGER protein, humanReceptor for Advanced Glycation End ProductsTGFB1 protein, humanTransforming Growth Factor beta1quantitative polymerase chain reactionreceptor for advanced glycation end productsTransforming growth factor-β1type 1 diabetesurinary albumin excretion rate

Identifiers

PMID32936764
PMCPMC7947732
OpenAlexW3084437172

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.