Evidence map›Paper›PMID 42473140›Full record

ArticleJournal of diabetes research2026

Expression Signatures of Vascular Complication-Associated Proteins in Type 2 Diabetes: A Multiomics Analysis From the FIELD Study.

Habib Francis, Andrzej S Januszewski, Abubakar S Mangani, Matthew B O Rourke, Michael L H Huang, Fahmida K Ema, Anandwardhan A Hardikar, Mugdha V Joglekar, David R Sullivan, Ronald C W Ma and 7 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of diabetes research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Article
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

17 authors.

Habib FrancisNHMRC Clinical Trials Centre, Faculty of Medicine and Health, The University of Sydney, Sydney, Australia, sydney.edu.au.ORCID https://orcid.org/0009-0009-1106-4118
Andrzej S JanuszewskiNHMRC Clinical Trials Centre, Faculty of Medicine and Health, The University of Sydney, Sydney, Australia, sydney.edu.au.ORCID https://orcid.org/0000-0003-0995-4524
Abubakar S ManganiNHMRC Clinical Trials Centre, Faculty of Medicine and Health, The University of Sydney, Sydney, Australia, sydney.edu.au.ORCID https://orcid.org/0000-0002-8715-9908
Matthew B O RourkeBowel Cancer and Biomarker Research Laboratory, School of Medical Sciences, Kolling Institute, The University of Sydney, St Leonards, Australia, sydney.edu.au.ORCID https://orcid.org/0000-0002-0552-2962
Michael L H HuangNHMRC Clinical Trials Centre, Faculty of Medicine and Health, The University of Sydney, Sydney, Australia, sydney.edu.au.ORCID https://orcid.org/0000-0003-0693-7833
Fahmida K EmaNHMRC Clinical Trials Centre, Faculty of Medicine and Health, The University of Sydney, Sydney, Australia, sydney.edu.au.ORCID https://orcid.org/0009-0003-7654-9016
Anandwardhan A HardikarWestern Sydney University School of Medicine, Campbelltown, Australia.ORCID https://orcid.org/0000-0001-5587-2090
Mugdha V JoglekarWestern Sydney University School of Medicine, Campbelltown, Australia.ORCID https://orcid.org/0000-0001-5346-2266
David R SullivanRoyal Prince Alfred Hospital, Camperdown, Australia, nsw.gov.au.ORCID https://orcid.org/0000-0003-3085-5627
Ronald C W MaDepartment of Medicine and Therapeutics and Li Ka Shing Institute of Health Sciences, Faculty of Medicine, Prince of Wales Hospital, The Chinese University of Hong Kong, Sha Tin, Hong Kong, China, cuhk.edu.hk.ORCID https://orcid.org/0000-0002-1227-803X
Sanjeev GalandeShiv Nadar Institution of Eminence, Gautam Buddha Nagar, Uttar Pradesh, India.ORCID https://orcid.org/0000-0002-7251-1905
Val GebskiNHMRC Clinical Trials Centre, Faculty of Medicine and Health, The University of Sydney, Sydney, Australia, sydney.edu.au.ORCID https://orcid.org/0000-0001-8748-1844
Michael D EmdenRoyal Brisbane and Women's Hospital, Brisbane, Queensland, Australia.ORCID https://orcid.org/0000-0002-0149-639X
R John SimesNHMRC Clinical Trials Centre, Faculty of Medicine and Health, The University of Sydney, Sydney, Australia, sydney.edu.au.ORCID https://orcid.org/0000-0002-3740-7563
Alicia J JenkinsNHMRC Clinical Trials Centre, Faculty of Medicine and Health, The University of Sydney, Sydney, Australia, sydney.edu.au.ORCID https://orcid.org/0000-0003-0583-3717
Mark P MolloyBowel Cancer and Biomarker Research Laboratory, School of Medical Sciences, Kolling Institute, The University of Sydney, St Leonards, Australia, sydney.edu.au.ORCID https://orcid.org/0000-0003-4679-5868
Anthony C KeechNHMRC Clinical Trials Centre, Faculty of Medicine and Health, The University of Sydney, Sydney, Australia, sydney.edu.au.ORCID https://orcid.org/0000-0002-9426-9136

Funding

Council of Australasian University LibrariansNational Health and Medical Research Council 1147897University of Sydney
6 · The paper itself

Abstract

aimsThe aim of the study is to integrate targeted transcriptomic analyses of previously identified biomarker proteins (proteomic findings) to better understand vascular complications (Cx) in Type 2 diabetes (T2D).

methodsTotal RNA was extracted from baseline citrate plasma samples of 543 individuals with T2D from the Fenofibrate Intervention and Event Lowering in Diabetes (FIELD) trial. Among these, 224 participants had microvascular Cx, 142 had macrovascular Cx (51 had both types of Cx) and 228 had no Cx (control group). mRNA expression was quantified using the OpenArray platform and group differences were analysed using ΔΔct values. Neutrophil elastase (NE) protein levels were measured in baseline plasma by ELISA.

resultsEleven genes were retained for focused analysis. For microCx, the largest gene expression differences were observed for clusterin (~2-fold upregulation) and integrin alpha-IIb (~50% downregulation), compared with the control group. For macroCx, clusterin exhibited the strongest upregulation (~2.5-fold), whereas apolipoprotein F showed the greatest downregulation (~20%). Comparative analysis of proteomic and transcriptomic data across study groups revealed that only 32% of gene expression differences were mirrored at the protein level. NE levels were highest in the microCx group and were significantly elevated versus control only in that group; NE levels also correlated inversely with circulating actin protein expression (R

conclusionCombining proteomic and targeted plasma transcriptomic data provides exploratory insights into biological processes associated with vascular complications in T2D and highlights NE as a candidate component of a proteolytic pathway for further investigation.

Indexed as

Diabetes Mellitus, Type 2Diabetic AngiopathiesAgedBiomarkersClusterinFemaleGene Expression ProfilingHumansLeukocyte ElastaseMaleMiddle AgedMultiomicsProteomicsTranscriptomeBiomarkersClusterinLeukocyte Elastasebiomarkersdiabetesneutrophil elastaseOpenArrayqPCR

Identifiers

PMID42473140
PMCPMC13382072

What Socratic 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 Socratic graph.