Evidence map›Paper›PMID 41533335›Full record

ArticleDiabetes care2026

Soluble Urokinase Plasminogen Activator Receptor (suPAR) Mediates the Impact of Diabetes on Adverse Outcomes in Coronary Artery Disease.

Shaimaa M Sakr, Shivang Desai, Jose Medina-Inojosa, Chang Liu, Alexander C Razavi, Adithya K Yadalam, Yi-An Ko, Taha Ahmed, Kristen A Harris, Jingwen Huang and 13 more

Abstract read
In one paragraph

Article in Diabetes care, 2026. 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. Trial
  2. 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

23 authors.

Shaimaa M SakrDivision of Cardiology, Department of Medicine, Emory University School of Medicine, Atlanta, GA.ORCID 0009-0005-3787-2018
Shivang DesaiDivision of Cardiology, Department of Medicine, Emory University School of Medicine, Atlanta, GA.
Jose Medina-InojosaDivision of Cardiology, Department of Medicine, Emory University School of Medicine, Atlanta, GA.
Chang LiuDepartment of Epidemiology, Rollins School of Public Health, Emory University, Atlanta, GA.
Alexander C RazaviDivision of Cardiology, Department of Medicine, Emory University School of Medicine, Atlanta, GA.
Adithya K YadalamDivision of Cardiology, Department of Medicine, Emory University School of Medicine, Atlanta, GA.
Yi-An KoDepartment of Biostatistics and Bioinformatics, Rollins School of Public Health, Emory University, Atlanta, GA.
Taha AhmedDivision of Cardiology, Department of Medicine, Emory University School of Medicine, Atlanta, GA.
Kristen A HarrisDivision of Cardiology, Department of Medicine, Emory University School of Medicine, Atlanta, GA.
Jingwen HuangDivision of Cardiology, Department of Medicine, Emory University School of Medicine, Atlanta, GA.
Rebecca YeboahDepartment of Development Practice, Laney Graduate School, Emory University, Atlanta, GA.
Nisreen HarounDivision of Cardiology, Department of Medicine, Emory University School of Medicine, Atlanta, GA.
Joy D HartsfieldDivision of Cardiology, Department of Medicine, Emory University School of Medicine, Atlanta, GA.
Muhammad OwaisDivision of Cardiology, Department of Medicine, Emory University School of Medicine, Atlanta, GA.
Rafia LodhiDivision of Cardiology, Department of Medicine, Emory University School of Medicine, Atlanta, GA.
Ahmed A EldaidamouniDivision of Cardiology, Department of Medicine, Emory University School of Medicine, Atlanta, GA.
Mahmoud Al KasemDivision of Cardiology, Department of Medicine, Emory University School of Medicine, Atlanta, GA.
Mohammed K AliHubert Department of Global Health, Rollins School of Public Health, Emory University, Atlanta, GA.ORCID 0000-0001-7266-2503
K M Venkat NarayanHubert Department of Global Health, Rollins School of Public Health, Emory University, Atlanta, GA.ORCID 0000-0001-8621-5405
Francisco J PasquelDivision of Endocrinology, Department of Medicine, Emory University School of Medicine, Atlanta, GA.ORCID 0000-0002-3845-6703
Nikhil TandonDepartment of Endocrinology & Metabolism, All India Institute of Medical Sciences, New Delhi, India.ORCID 0000-0003-4604-1986
Viswanathan MohanDepartment of Diabetology, Dr. Mohan's Diabetes Specialities Centre, Madras Diabetes Research Foundation, Chennai, India.ORCID 0000-0001-5038-6210
Arshed A QuyyumiDivision of Cardiology, Department of Medicine, Emory University School of Medicine, Atlanta, GA.ORCID 0000-0002-8166-679X

Funding

Abbott LaboratoriesNIH HHS 1R01HL166004-01NIH HHS 3R01HL157311-03S1NIH HHS 5R01HL158141-043NIH HHS 5T32 HL130025NIH HHS P01HL154996-01A1NIH HHS P30DK111024-07S2NIH HHS R01HL166004-01NIH HHS R33HL138657-05
6 · The paper itself

Abstract

objectiveType 2 diabetes (T2D) is a significant risk factor for adverse outcomes in coronary heart disease (CHD). We investigated whether inflammation and immune dysregulation, measured using soluble urokinase plasminogen activator receptor (suPAR) and high-sensitivity C-reactive protein (hs-CRP) levels, mediate this risk. RESEARCH DESIGN AND

methodsPatients with and without CHD enrolled in the Emory Cardiovascular Biobank had suPAR (ViroGates, Denmark) and hs-CRP levels measured and were followed for 1) cardiovascular death, 2) a composite of incident myocardial infarction and cardiovascular death, and 3) all-cause death. Fine and Gray or Cox proportional hazards models adjusted for demographic, clinical, and treatment variables were used. Regression-based causal mediation analyses were performed.

resultsA total of 4,324 participants (mean [SD] age 64 [11.9] years, 36% women, 31.8% with T2D) were followed for a median of 6.9 years. SuPAR levels were higher in those with T2D (median [interquartile range] 3,260 [2,503-4,463] vs. 2,792 [2,217-3,600] pg/mL). T2D was associated with a higher adjusted risk (hazard ratio [HR] 1.38; 95% CI 1.16, 1.63; P < 0.001) of cardiovascular death that was greatly attenuated (HR 1.18; 95% CI 0.99, 1.40; P = 0.1) after adjustment for suPAR, but not hs-CRP, levels. Similar findings were observed for the other outcomes. SuPAR, but not hs-CRP, levels mediated >50% of the effect of T2D on adverse outcomes.

conclusionsThe impact of T2D on adverse outcomes is significantly mediated through chronic inflammation and immune dysregulation, estimated using suPAR levels. Whether novel therapies for reducing suPAR levels will impact CHD risk in T2D warrants further investigation.

Indexed as

Coronary DiseaseC-Reactive ProteinDiabetes Mellitus, Type 2Receptors, Urokinase Plasminogen ActivatorAgedBiological Specimen BanksCause of DeathFemaleHumansImmune System PhenomenaInflammationMaleMiddle AgedProportional Hazards ModelsC-Reactive ProteinReceptors, Urokinase Plasminogen Activator

Identifiers

PMID41533335
PMCPMC12925993

What OpenQuestion holds

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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.