<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Canonico F</submitter><funding>British Heart Foundation</funding><funding>European Research Council</funding><pagination>2653-2662</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC10730239</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>119(16)</volume><pubmed_abstract>&lt;h4>Aims&lt;/h4>The functional capacity of the immune cells is strongly dependent on their metabolic state and inflammatory responses are characterized by a greater use of glucose in immune cells. This study is aimed to establish the role of glucose metabolism and its players [glucose transporter 1 (GLUT-1) and pyruvate kinase isozyme M2 (PKM2)] in the dysregulation of adaptive immunity and inflammation observed in patients with non-ST-segment elevation myocardial infarction (NSTEMI).&lt;h4>Methods and results&lt;/h4>We enrolled 248 patients allocated to three groups: NSTEMI patients, chronic coronary syndromes (CCS) patients, healthy subjects (HSs). NSTEMI patients showed higher expression of GLUT-1 and an enhanced glucose uptake in T cells when compared with CCS patients (P &lt; 0.0001; P = 0.0101, </pubmed_abstract><journal>Cardiovascular research</journal><pubmed_title>GLUT-1/PKM2 loop dysregulation in patients with non-ST-segment elevation myocardial infarction promotes metainflammation.</pubmed_title><pmcid>PMC10730239</pmcid><funding_grant_id>PG/19/84/34771</funding_grant_id><funding_grant_id>FS/4yPhD/F/20/34127A, PG/19/84/34771, FS/19/56/34893A, PG/21/10541, PG/21/10634</funding_grant_id><funding_grant_id>726318</funding_grant_id><funding_grant_id>ERC-CoG-726318</funding_grant_id><pubmed_authors>Di Sario M</pubmed_authors><pubmed_authors>Liuzzo G</pubmed_authors><pubmed_authors>d'Aiello A</pubmed_authors><pubmed_authors>Pedicino D</pubmed_authors><pubmed_authors>Angelini G</pubmed_authors><pubmed_authors>Severino A</pubmed_authors><pubmed_authors>Wierzbicki K</pubmed_authors><pubmed_authors>D'Amario D</pubmed_authors><pubmed_authors>Canonico F</pubmed_authors><pubmed_authors>Ciampi P</pubmed_authors><pubmed_authors>Montone RA</pubmed_authors><pubmed_authors>Massetti M</pubmed_authors><pubmed_authors>Russo S</pubmed_authors><pubmed_authors>De Ciutiis A</pubmed_authors><pubmed_authors>Baldi A</pubmed_authors><pubmed_authors>Vinci R</pubmed_authors><pubmed_authors>Ponzo M</pubmed_authors><pubmed_authors>Szczepaniak P</pubmed_authors><pubmed_authors>Flego D</pubmed_authors><pubmed_authors>Bonanni A</pubmed_authors><pubmed_authors>Pisano E</pubmed_authors><pubmed_authors>Crea F</pubmed_authors><pubmed_authors>Kapelak B</pubmed_authors><pubmed_authors>Guzik TJ</pubmed_authors></additional><is_claimable>false</is_claimable><name>GLUT-1/PKM2 loop dysregulation in patients with non-ST-segment elevation myocardial infarction promotes metainflammation.</name><description>&lt;h4>Aims&lt;/h4>The functional capacity of the immune cells is strongly dependent on their metabolic state and inflammatory responses are characterized by a greater use of glucose in immune cells. This study is aimed to establish the role of glucose metabolism and its players [glucose transporter 1 (GLUT-1) and pyruvate kinase isozyme M2 (PKM2)] in the dysregulation of adaptive immunity and inflammation observed in patients with non-ST-segment elevation myocardial infarction (NSTEMI).&lt;h4>Methods and results&lt;/h4>We enrolled 248 patients allocated to three groups: NSTEMI patients, chronic coronary syndromes (CCS) patients, healthy subjects (HSs). NSTEMI patients showed higher expression of GLUT-1 and an enhanced glucose uptake in T cells when compared with CCS patients (P &lt; 0.0001; P = 0.0101, </description><dates><release>2023-01-01T00:00:00Z</release><publication>2023 Dec</publication><modification>2025-04-22T08:20:29.27Z</modification><creation>2024-11-21T06:44:03.971Z</creation></dates><accession>S-EPMC10730239</accession><cross_references><pubmed>36508576</pubmed><doi>10.1093/cvr/cvac184</doi></cross_references></HashMap>