<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Sakr SM</submitter><funding>Abbott Laboratories</funding><funding>NIH HHS</funding><pagination>450-459</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC12925993</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>49(3)</volume><pubmed_abstract>&lt;h4>Objective&lt;/h4>Type 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.&lt;h4>Research design and methods&lt;/h4>Patients 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 mediatio</pubmed_abstract><journal>Diabetes care</journal><pubmed_title>Soluble Urokinase Plasminogen Activator Receptor (suPAR) Mediates the Impact of Diabetes on Adverse Outcomes in Coronary Artery Disease.</pubmed_title><pmcid>PMC12925993</pmcid><funding_grant_id>3R01HL157311-03S1</funding_grant_id><funding_grant_id>P01HL154996-01A1</funding_grant_id><funding_grant_id>5T32 HL130025</funding_grant_id><funding_grant_id>P30DK111024-07S2</funding_grant_id><funding_grant_id>R01HL166004-01</funding_grant_id><funding_grant_id>5R01HL158141-043</funding_grant_id><funding_grant_id>1R01HL166004-01</funding_grant_id><funding_grant_id>R33HL138657-05</funding_grant_id><pubmed_authors>Lodhi R</pubmed_authors><pubmed_authors>Eldaidamouni AA</pubmed_authors><pubmed_authors>Ahmed T</pubmed_authors><pubmed_authors>Huang J</pubmed_authors><pubmed_authors>Sakr SM</pubmed_authors><pubmed_authors>Pasquel FJ</pubmed_authors><pubmed_authors>Medina-Inojosa J</pubmed_authors><pubmed_authors>Quyyumi AA</pubmed_authors><pubmed_authors>Yadalam AK</pubmed_authors><pubmed_authors>Ali MK</pubmed_authors><pubmed_authors>Desai S</pubmed_authors><pubmed_authors>Harris KA</pubmed_authors><pubmed_authors>Yeboah R</pubmed_authors><pubmed_authors>Haroun N</pubmed_authors><pubmed_authors>Razavi AC</pubmed_authors><pubmed_authors>Owais M</pubmed_authors><pubmed_authors>Ko YA</pubmed_authors><pubmed_authors>Mohan V</pubmed_authors><pubmed_authors>Tandon N</pubmed_authors><pubmed_authors>Al Kasem M</pubmed_authors><pubmed_authors>Liu C</pubmed_authors><pubmed_authors>Narayan KMV</pubmed_authors><pubmed_authors>Hartsfield JD</pubmed_authors></additional><is_claimable>false</is_claimable><name>Soluble Urokinase Plasminogen Activator Receptor (suPAR) Mediates the Impact of Diabetes on Adverse Outcomes in Coronary Artery Disease.</name><description>&lt;h4>Objective&lt;/h4>Type 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.&lt;h4>Research design and methods&lt;/h4>Patients 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 mediatio</description><dates><release>2026-01-01T00:00:00Z</release><publication>2026 Mar</publication><modification>2026-07-16T18:34:02.445Z</modification><creation>2026-07-11T03:08:33.4Z</creation></dates><accession>S-EPMC12925993</accession><cross_references><pubmed>41533335</pubmed><doi>10.2337/dc25-0940</doi></cross_references></HashMap>