Sodium-glucose cotransporter 2 inhibitors induce anti-inflammatory and anti-ferroptotic shift in epicardial adipose tissue of subjects with severe heart failure
Sodium-glucose cotransporter 2 inhibitors (SGLT-2i) are glucose-lowering agents used for the treatment of type 2 diabetes mellitus, which also improve heart failure and decrease the risk of cardiovascular complications. Epicardial adipose tissue (EAT) dysfunction was suggested to contribute to the d...
Saved in:
| Published in | Cardiovascular diabetology Vol. 23; no. 1; pp. 223 - 17 |
|---|---|
| Main Authors | , , , , , , , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
England
BioMed Central
28.06.2024
BMC |
| Subjects | |
| Online Access | Get full text |
Cover
Loading…
| Abstract | Sodium-glucose cotransporter 2 inhibitors (SGLT-2i) are glucose-lowering agents used for the treatment of type 2 diabetes mellitus, which also improve heart failure and decrease the risk of cardiovascular complications. Epicardial adipose tissue (EAT) dysfunction was suggested to contribute to the development of heart failure. We aimed to elucidate a possible role of changes in EAT metabolic and inflammatory profile in the beneficial cardioprotective effects of SGLT-2i in subjects with severe heart failure.
26 subjects with severe heart failure, with reduced ejection fraction, treated with SGLT-2i versus 26 subjects without treatment, matched for age (54.0 ± 2.1 vs. 55.3 ± 2.1 years, n.s.), body mass index (27.8 ± 0.9 vs. 28.8 ± 1.0 kg/m
, n.s.) and left ventricular ejection fraction (20.7 ± 0.5 vs. 23.2 ± 1.7%, n.s.), who were scheduled for heart transplantation or mechanical support implantation, were included in the study. A complex metabolomic and gene expression analysis of EAT obtained during surgery was performed.
SGLT-2i ameliorated inflammation, as evidenced by the improved gene expression profile of pro-inflammatory genes in adipose tissue and decreased infiltration of immune cells into EAT. Enrichment of ether lipids with oleic acid noted on metabolomic analysis suggests a reduced disposition to ferroptosis, potentially further contributing to decreased oxidative stress in EAT of SGLT-2i treated subjects.
Our results show decreased inflammation in EAT of patients with severe heart failure treated by SGLT-2i, as compared to patients with heart failure without this therapy. Modulation of EAT inflammatory and metabolic status could represent a novel mechanism behind SGLT-2i-associated cardioprotective effects in patients with heart failure. |
|---|---|
| AbstractList | Sodium-glucose cotransporter 2 inhibitors (SGLT-2i) are glucose-lowering agents used for the treatment of type 2 diabetes mellitus, which also improve heart failure and decrease the risk of cardiovascular complications. Epicardial adipose tissue (EAT) dysfunction was suggested to contribute to the development of heart failure. We aimed to elucidate a possible role of changes in EAT metabolic and inflammatory profile in the beneficial cardioprotective effects of SGLT-2i in subjects with severe heart failure.
26 subjects with severe heart failure, with reduced ejection fraction, treated with SGLT-2i versus 26 subjects without treatment, matched for age (54.0 ± 2.1 vs. 55.3 ± 2.1 years, n.s.), body mass index (27.8 ± 0.9 vs. 28.8 ± 1.0 kg/m
, n.s.) and left ventricular ejection fraction (20.7 ± 0.5 vs. 23.2 ± 1.7%, n.s.), who were scheduled for heart transplantation or mechanical support implantation, were included in the study. A complex metabolomic and gene expression analysis of EAT obtained during surgery was performed.
SGLT-2i ameliorated inflammation, as evidenced by the improved gene expression profile of pro-inflammatory genes in adipose tissue and decreased infiltration of immune cells into EAT. Enrichment of ether lipids with oleic acid noted on metabolomic analysis suggests a reduced disposition to ferroptosis, potentially further contributing to decreased oxidative stress in EAT of SGLT-2i treated subjects.
Our results show decreased inflammation in EAT of patients with severe heart failure treated by SGLT-2i, as compared to patients with heart failure without this therapy. Modulation of EAT inflammatory and metabolic status could represent a novel mechanism behind SGLT-2i-associated cardioprotective effects in patients with heart failure. Abstract Background Sodium-glucose cotransporter 2 inhibitors (SGLT-2i) are glucose-lowering agents used for the treatment of type 2 diabetes mellitus, which also improve heart failure and decrease the risk of cardiovascular complications. Epicardial adipose tissue (EAT) dysfunction was suggested to contribute to the development of heart failure. We aimed to elucidate a possible role of changes in EAT metabolic and inflammatory profile in the beneficial cardioprotective effects of SGLT-2i in subjects with severe heart failure. Methods 26 subjects with severe heart failure, with reduced ejection fraction, treated with SGLT-2i versus 26 subjects without treatment, matched for age (54.0 ± 2.1 vs. 55.3 ± 2.1 years, n.s.), body mass index (27.8 ± 0.9 vs. 28.8 ± 1.0 kg/m2, n.s.) and left ventricular ejection fraction (20.7 ± 0.5 vs. 23.2 ± 1.7%, n.s.), who were scheduled for heart transplantation or mechanical support implantation, were included in the study. A complex metabolomic and gene expression analysis of EAT obtained during surgery was performed. Results SGLT-2i ameliorated inflammation, as evidenced by the improved gene expression profile of pro-inflammatory genes in adipose tissue and decreased infiltration of immune cells into EAT. Enrichment of ether lipids with oleic acid noted on metabolomic analysis suggests a reduced disposition to ferroptosis, potentially further contributing to decreased oxidative stress in EAT of SGLT-2i treated subjects. Conclusions Our results show decreased inflammation in EAT of patients with severe heart failure treated by SGLT-2i, as compared to patients with heart failure without this therapy. Modulation of EAT inflammatory and metabolic status could represent a novel mechanism behind SGLT-2i-associated cardioprotective effects in patients with heart failure. BackgroundSodium-glucose cotransporter 2 inhibitors (SGLT-2i) are glucose-lowering agents used for the treatment of type 2 diabetes mellitus, which also improve heart failure and decrease the risk of cardiovascular complications. Epicardial adipose tissue (EAT) dysfunction was suggested to contribute to the development of heart failure. We aimed to elucidate a possible role of changes in EAT metabolic and inflammatory profile in the beneficial cardioprotective effects of SGLT-2i in subjects with severe heart failure.Methods26 subjects with severe heart failure, with reduced ejection fraction, treated with SGLT-2i versus 26 subjects without treatment, matched for age (54.0 ± 2.1 vs. 55.3 ± 2.1 years, n.s.), body mass index (27.8 ± 0.9 vs. 28.8 ± 1.0 kg/m2, n.s.) and left ventricular ejection fraction (20.7 ± 0.5 vs. 23.2 ± 1.7%, n.s.), who were scheduled for heart transplantation or mechanical support implantation, were included in the study. A complex metabolomic and gene expression analysis of EAT obtained during surgery was performed.ResultsSGLT-2i ameliorated inflammation, as evidenced by the improved gene expression profile of pro-inflammatory genes in adipose tissue and decreased infiltration of immune cells into EAT. Enrichment of ether lipids with oleic acid noted on metabolomic analysis suggests a reduced disposition to ferroptosis, potentially further contributing to decreased oxidative stress in EAT of SGLT-2i treated subjects.ConclusionsOur results show decreased inflammation in EAT of patients with severe heart failure treated by SGLT-2i, as compared to patients with heart failure without this therapy. Modulation of EAT inflammatory and metabolic status could represent a novel mechanism behind SGLT-2i-associated cardioprotective effects in patients with heart failure. Sodium-glucose cotransporter 2 inhibitors (SGLT-2i) are glucose-lowering agents used for the treatment of type 2 diabetes mellitus, which also improve heart failure and decrease the risk of cardiovascular complications. Epicardial adipose tissue (EAT) dysfunction was suggested to contribute to the development of heart failure. We aimed to elucidate a possible role of changes in EAT metabolic and inflammatory profile in the beneficial cardioprotective effects of SGLT-2i in subjects with severe heart failure.BACKGROUNDSodium-glucose cotransporter 2 inhibitors (SGLT-2i) are glucose-lowering agents used for the treatment of type 2 diabetes mellitus, which also improve heart failure and decrease the risk of cardiovascular complications. Epicardial adipose tissue (EAT) dysfunction was suggested to contribute to the development of heart failure. We aimed to elucidate a possible role of changes in EAT metabolic and inflammatory profile in the beneficial cardioprotective effects of SGLT-2i in subjects with severe heart failure.26 subjects with severe heart failure, with reduced ejection fraction, treated with SGLT-2i versus 26 subjects without treatment, matched for age (54.0 ± 2.1 vs. 55.3 ± 2.1 years, n.s.), body mass index (27.8 ± 0.9 vs. 28.8 ± 1.0 kg/m2, n.s.) and left ventricular ejection fraction (20.7 ± 0.5 vs. 23.2 ± 1.7%, n.s.), who were scheduled for heart transplantation or mechanical support implantation, were included in the study. A complex metabolomic and gene expression analysis of EAT obtained during surgery was performed.METHODS26 subjects with severe heart failure, with reduced ejection fraction, treated with SGLT-2i versus 26 subjects without treatment, matched for age (54.0 ± 2.1 vs. 55.3 ± 2.1 years, n.s.), body mass index (27.8 ± 0.9 vs. 28.8 ± 1.0 kg/m2, n.s.) and left ventricular ejection fraction (20.7 ± 0.5 vs. 23.2 ± 1.7%, n.s.), who were scheduled for heart transplantation or mechanical support implantation, were included in the study. A complex metabolomic and gene expression analysis of EAT obtained during surgery was performed.SGLT-2i ameliorated inflammation, as evidenced by the improved gene expression profile of pro-inflammatory genes in adipose tissue and decreased infiltration of immune cells into EAT. Enrichment of ether lipids with oleic acid noted on metabolomic analysis suggests a reduced disposition to ferroptosis, potentially further contributing to decreased oxidative stress in EAT of SGLT-2i treated subjects.RESULTSSGLT-2i ameliorated inflammation, as evidenced by the improved gene expression profile of pro-inflammatory genes in adipose tissue and decreased infiltration of immune cells into EAT. Enrichment of ether lipids with oleic acid noted on metabolomic analysis suggests a reduced disposition to ferroptosis, potentially further contributing to decreased oxidative stress in EAT of SGLT-2i treated subjects.Our results show decreased inflammation in EAT of patients with severe heart failure treated by SGLT-2i, as compared to patients with heart failure without this therapy. Modulation of EAT inflammatory and metabolic status could represent a novel mechanism behind SGLT-2i-associated cardioprotective effects in patients with heart failure.CONCLUSIONSOur results show decreased inflammation in EAT of patients with severe heart failure treated by SGLT-2i, as compared to patients with heart failure without this therapy. Modulation of EAT inflammatory and metabolic status could represent a novel mechanism behind SGLT-2i-associated cardioprotective effects in patients with heart failure. |
| ArticleNumber | 223 |
| Author | Modos, Istvan Ivak, Peter Stranecky, Viktor Netuka, Ivan Kasperova, Barbora Judita Riecan, Martin Stemberkova Hubackova, Sona Kratochvilova, Helena Janovska, Petra Kobets, Tatyana Cajka, Tomas Haluzik, Martin Mraz, Milos Kuda, Ondrej Vrzackova, Nikola Svoboda, Petr Hlavacek, Daniel Steiner Mrazova, Lenka Melenovsky, Vojtech Mahrik, Jakub |
| Author_xml | – sequence: 1 givenname: Barbora Judita orcidid: 0000-0003-4578-1093 surname: Kasperova fullname: Kasperova, Barbora Judita – sequence: 2 givenname: Milos orcidid: 0000-0001-5322-4612 surname: Mraz fullname: Mraz, Milos – sequence: 3 givenname: Petr orcidid: 0000-0001-7297-4208 surname: Svoboda fullname: Svoboda, Petr – sequence: 4 givenname: Daniel orcidid: 0000-0001-8453-1666 surname: Hlavacek fullname: Hlavacek, Daniel – sequence: 5 givenname: Helena orcidid: 0000-0001-8264-3883 surname: Kratochvilova fullname: Kratochvilova, Helena – sequence: 6 givenname: Istvan orcidid: 0000-0003-4692-1625 surname: Modos fullname: Modos, Istvan – sequence: 7 givenname: Nikola orcidid: 0000-0002-9108-3053 surname: Vrzackova fullname: Vrzackova, Nikola – sequence: 8 givenname: Peter orcidid: 0000-0002-1803-604X surname: Ivak fullname: Ivak, Peter – sequence: 9 givenname: Petra orcidid: 0000-0002-6154-2175 surname: Janovska fullname: Janovska, Petra – sequence: 10 givenname: Tatyana orcidid: 0000-0003-0294-3638 surname: Kobets fullname: Kobets, Tatyana – sequence: 11 givenname: Jakub orcidid: 0000-0002-9163-1881 surname: Mahrik fullname: Mahrik, Jakub – sequence: 12 givenname: Martin orcidid: 0000-0001-6251-1277 surname: Riecan fullname: Riecan, Martin – sequence: 13 givenname: Lenka orcidid: 0000-0003-4347-7768 surname: Steiner Mrazova fullname: Steiner Mrazova, Lenka – sequence: 14 givenname: Viktor orcidid: 0000-0002-2599-6479 surname: Stranecky fullname: Stranecky, Viktor – sequence: 15 givenname: Ivan orcidid: 0000-0002-1567-7036 surname: Netuka fullname: Netuka, Ivan – sequence: 16 givenname: Tomas orcidid: 0000-0002-9728-3355 surname: Cajka fullname: Cajka, Tomas – sequence: 17 givenname: Ondrej orcidid: 0000-0001-7034-4536 surname: Kuda fullname: Kuda, Ondrej – sequence: 18 givenname: Vojtech orcidid: 0000-0001-8921-7078 surname: Melenovsky fullname: Melenovsky, Vojtech – sequence: 19 givenname: Sona orcidid: 0000-0002-3454-6840 surname: Stemberkova Hubackova fullname: Stemberkova Hubackova, Sona – sequence: 20 givenname: Martin orcidid: 0000-0002-0201-6888 surname: Haluzik fullname: Haluzik, Martin |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/38943140$$D View this record in MEDLINE/PubMed |
| BookMark | eNp9kstu1TAQhiNURC_wAiyQJTZsAr4ltpeo4lKpEgtgbU2ccY-PkjjYDqhvw6Pi01Mq1AULy9bv7x-PNf95c7LEBZvmJaNvGdP9u8y4EaKlXNbFjW7Nk-aMSdW1XEt68s_5tDnPeU8pU7pnz5pToY0UTNKz5vfXOIZtbm-mzcWMxMWSYMlrTAUT4SQsuzCEElOux3FzSGApoQ2Ln2CeoV7cVmU8qh5TimuJJTiSd8GX6iG4BgdpDDARGMN6eKSEnDck0ZO8DXt0JZNfoexIxp-YkOwQUiEewrQlfN489TBlfHG_XzTfP374dvm5vf7y6ery_XXrpGSl9dSh0cC9lkC5GLVBL70ZqiyEBy961jvjXdd1auykp0OvPYdOeaW45ygumqtj3THC3q4pzJBubYRg74SYbmztKrgJre8GNZjBAaCUMFLde2Gk9oOQnVTjUGu9OdZaU_yxYS52DtnhNMGCcctWUCUU471UFX39CN3HLS31pwfK8Do9riv16p7ahhnHh_b-zrEC_Ai4FHNO6B8QRu0hLPYYFlvDYu_CYk016UcmFwqUEJeagTD9z_oHkwrHbA |
| CitedBy_id | crossref_primary_10_1186_s12933_024_02539_x crossref_primary_10_1038_s41392_024_01951_9 crossref_primary_10_1186_s12933_024_02517_3 crossref_primary_10_1016_j_phrs_2024_107505 |
| Cites_doi | 10.1016/j.mce.2015.08.025 10.1002/ejhf.1858 10.1016/j.bbalip.2019.158576 10.1016/j.jacc.2011.01.048 10.1056/NEJMoa2022190 10.1016/j.cardfail.2015.07.014 10.3390/cells10082150 10.1016/j.phrs.2022.106448 10.1093/nar/gkad960 10.1038/nm.1964 10.1186/s12933-021-01237-2 10.1038/s41419-023-05708-0 10.1002/oby.22798 10.33549/physiolres.933036 10.3389/fphar.2023.1078205 10.1016/j.bbalip.2017.11.004 10.1126/sciadv.abb7272 10.1186/s13059-014-0550-8 10.1016/j.freeradbiomed.2017.01.035 10.1186/s12933-023-01814-7 10.1016/j.semcancer.2018.07.009 10.1016/j.celrep.2020.02.049 10.3389/fcvm.2021.720690 10.1016/j.metabol.2023.155659 10.3389/fphar.2022.1045235 10.3389/fimmu.2023.1126997 10.1530/EC-21-0558 10.1038/75556 10.1093/genetics/iyad031 10.1016/j.diabres.2022.109927 10.1016/j.jacc.2018.03.509 10.1002/jcsm.12631 10.1093/nar/gkab382 10.1016/j.jacep.2017.03.002 10.1016/j.jchromb.2019.03.006 10.1093/nar/gky1032 10.1021/jacs.7b00390 10.1186/s12933-021-01346-y 10.1016/j.metabol.2021.154936 10.1002/ejhf.1617 10.1111/jcmm.14758 10.1186/s12933-019-0947-5 10.1093/nar/gkad1025 10.1056/NEJMoa1504720 10.1161/ATVBAHA.122.317840 10.1016/j.ebiom.2017.05.028 10.1038/s41589-022-01249-3 10.1038/s41467-019-10711-1 10.1002/ejhf.2709 10.1056/NEJMoa2107038 10.1093/nar/gkac958 10.1056/NEJMoa1812389 10.1016/j.biopha.2023.114535 10.1371/journal.pbio.0060184 10.1161/01.CIR.0000099542.57313.C5 10.3390/ijms24076838 10.21037/amj.2020.03.03 10.1016/j.jjcc.2016.08.016 10.1111/dom.14596 10.1016/j.ahj.2007.03.019 10.1016/j.metabol.2020.154452 10.1016/j.jacc.2017.04.025 10.1016/j.molcel.2015.06.011 10.1186/s12933-017-0658-8 10.1002/ejhf.2337 10.1016/j.freeradbiomed.2019.01.008 10.1016/j.recesp.2021.11.027 10.1016/j.jchf.2020.06.003 10.1002/ejhf.2115 10.1113/JP273049 10.1056/NEJMoa1911303 10.1186/s13098-017-0275-4 10.1093/cvr/cvx186 10.1007/s40618-021-01687-1 10.1155/2022/8373389 10.3390/cells12060867 10.1093/ehjcvp/pvab056 10.1161/ATVBAHA.120.313955 10.1038/ncpcardio0319 10.1056/NEJMoa2206286 10.1016/j.yjmcc.2022.03.005 10.1186/1532-429X-12-40 10.2337/db15-0399 |
| ContentType | Journal Article |
| Copyright | 2024. The Author(s). 2024. This work is licensed under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. |
| Copyright_xml | – notice: 2024. The Author(s). – notice: 2024. This work is licensed under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. |
| DBID | AAYXX CITATION CGR CUY CVF ECM EIF NPM 3V. 7T5 7X7 7XB 88E 8FI 8FJ 8FK ABUWG AFKRA AZQEC BENPR CCPQU DWQXO FYUFA GHDGH H94 K9. M0S M1P PHGZM PHGZT PIMPY PJZUB PKEHL PPXIY PQEST PQQKQ PQUKI PRINS 7X8 DOA |
| DOI | 10.1186/s12933-024-02298-9 |
| DatabaseName | CrossRef Medline MEDLINE MEDLINE (Ovid) MEDLINE MEDLINE PubMed ProQuest Central (Corporate) Immunology Abstracts Health & Medical Collection ProQuest Central (purchase pre-March 2016) Medical Database (Alumni Edition) ProQuest Hospital Collection Hospital Premium Collection (Alumni Edition) ProQuest Central (Alumni) (purchase pre-March 2016) ProQuest Central (Alumni) ProQuest Central UK/Ireland ProQuest Central Essentials ProQuest Central ProQuest One Community College ProQuest Central Korea Health Research Premium Collection Health Research Premium Collection (Alumni) AIDS and Cancer Research Abstracts ProQuest Health & Medical Complete (Alumni) Health & Medical Collection (Alumni) Medical Database ProQuest Central Premium ProQuest One Academic (New) ProQuest - Publicly Available Content Database ProQuest Health & Medical Research Collection ProQuest One Academic Middle East (New) ProQuest One Health & Nursing ProQuest One Academic Eastern Edition (DO NOT USE) ProQuest One Academic ProQuest One Academic UKI Edition ProQuest Central China MEDLINE - Academic DOAJ Directory of Open Access Journals |
| DatabaseTitle | CrossRef MEDLINE Medline Complete MEDLINE with Full Text PubMed MEDLINE (Ovid) Publicly Available Content Database ProQuest One Academic Middle East (New) ProQuest Central Essentials ProQuest Health & Medical Complete (Alumni) ProQuest Central (Alumni Edition) ProQuest One Community College ProQuest One Health & Nursing ProQuest Central China ProQuest Central Health Research Premium Collection Health and Medicine Complete (Alumni Edition) ProQuest Central Korea Health & Medical Research Collection AIDS and Cancer Research Abstracts ProQuest Central (New) ProQuest Medical Library (Alumni) ProQuest One Academic Eastern Edition ProQuest Hospital Collection Health Research Premium Collection (Alumni) ProQuest Hospital Collection (Alumni) ProQuest Health & Medical Complete ProQuest Medical Library ProQuest One Academic UKI Edition Immunology Abstracts ProQuest One Academic ProQuest One Academic (New) ProQuest Central (Alumni) MEDLINE - Academic |
| DatabaseTitleList | MEDLINE Publicly Available Content Database MEDLINE - Academic |
| Database_xml | – sequence: 1 dbid: DOA name: DOAJ Directory of Open Access Journals url: https://www.doaj.org/ sourceTypes: Open Website – sequence: 2 dbid: NPM name: PubMed url: https://proxy.k.utb.cz/login?url=http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed sourceTypes: Index Database – sequence: 3 dbid: EIF name: MEDLINE url: https://proxy.k.utb.cz/login?url=https://www.webofscience.com/wos/medline/basic-search sourceTypes: Index Database – sequence: 4 dbid: BENPR name: ProQuest Central url: https://www.proquest.com/central sourceTypes: Aggregation Database |
| DeliveryMethod | fulltext_linktorsrc |
| Discipline | Medicine |
| EISSN | 1475-2840 |
| EndPage | 17 |
| ExternalDocumentID | oai_doaj_org_article_f5b7b9bcaae44ad086f3948fb34547db 38943140 10_1186_s12933_024_02298_9 |
| Genre | Research Support, Non-U.S. Gov't Journal Article |
| GeographicLocations | United States--US Germany |
| GeographicLocations_xml | – name: United States--US – name: Germany |
| GrantInformation_xml | – fundername: CZ - DRO (Institute for Clinical and Experimental Medicine- IKEM) grantid: IN 00023001 – fundername: National Institute for Research of Metabolic and Cardiovascular Diseases grantid: Programme EXCELES, ID Project No. LX22NPO5104 - Funded by the European Union- Next Generation EU – fundername: Ministerstvo Zdravotnictví Ceské Republiky grantid: NV19-02-00118 |
| GroupedDBID | --- 0R~ 29B 2WC 53G 5GY 5VS 6J9 7X7 88E 8FI 8FJ AAFWJ AAJSJ AASML AAYXX ABDBF ABUWG ACGFO ACGFS ACIHN ACIWK ACPRK ACUHS ADBBV ADRAZ ADUKV AEAQA AENEX AFKRA AFPKN AFRAH AHBYD AHMBA AHYZX ALIPV ALMA_UNASSIGNED_HOLDINGS AMKLP AMTXH AOIJS BAPOH BAWUL BCNDV BENPR BFQNJ BMC BPHCQ BVXVI C6C CCPQU CITATION CS3 DIK DU5 E3Z EAD EAP EAS EBD EBLON EBS EMB EMK EMOBN ESX F5P FYUFA GROUPED_DOAJ GX1 HMCUK HYE IAO IHR INH INR ITC KQ8 M1P M48 M~E O5R O5S OK1 OVT P2P PGMZT PHGZM PHGZT PIMPY PQQKQ PROAC PSQYO RBZ RNS ROL RPM RSV SMD SOJ SV3 TR2 TUS UKHRP W2D WOQ WOW XSB CGR CUY CVF ECM EIF NPM 3V. 7T5 7XB 8FK AZQEC DWQXO H94 K9. PJZUB PKEHL PPXIY PQEST PQUKI PRINS 7X8 PUEGO |
| ID | FETCH-LOGICAL-c441t-f0ce98a2f84a023d89ef4f9b0ce33faf3616c9fc5557d54f0b68f2a57f772f2e3 |
| IEDL.DBID | M48 |
| ISSN | 1475-2840 |
| IngestDate | Wed Aug 27 01:11:56 EDT 2025 Mon Jul 21 10:37:36 EDT 2025 Sat Jul 26 03:20:24 EDT 2025 Thu Apr 03 06:59:00 EDT 2025 Tue Jul 01 04:20:03 EDT 2025 Thu Apr 24 22:58:25 EDT 2025 |
| IsDoiOpenAccess | true |
| IsOpenAccess | true |
| IsPeerReviewed | true |
| IsScholarly | true |
| Issue | 1 |
| Keywords | Heart failure Ether lipids Inflammation Adipose tissue Sodium-glucose cotransporter 2 inhibitors |
| Language | English |
| License | 2024. The Author(s). |
| LinkModel | DirectLink |
| MergedId | FETCHMERGED-LOGICAL-c441t-f0ce98a2f84a023d89ef4f9b0ce33faf3616c9fc5557d54f0b68f2a57f772f2e3 |
| Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 content type line 23 |
| ORCID | 0000-0002-9108-3053 0000-0001-8921-7078 0000-0001-8453-1666 0000-0001-7297-4208 0000-0002-1803-604X 0000-0001-7034-4536 0000-0002-2599-6479 0000-0001-5322-4612 0000-0002-0201-6888 0000-0002-9728-3355 0000-0003-4578-1093 0000-0001-8264-3883 0000-0003-4347-7768 0000-0002-9163-1881 0000-0001-6251-1277 0000-0002-1567-7036 0000-0003-0294-3638 0000-0003-4692-1625 0000-0002-3454-6840 0000-0002-6154-2175 |
| OpenAccessLink | https://doaj.org/article/f5b7b9bcaae44ad086f3948fb34547db |
| PMID | 38943140 |
| PQID | 3079228428 |
| PQPubID | 42570 |
| PageCount | 17 |
| ParticipantIDs | doaj_primary_oai_doaj_org_article_f5b7b9bcaae44ad086f3948fb34547db proquest_miscellaneous_3073712647 proquest_journals_3079228428 pubmed_primary_38943140 crossref_primary_10_1186_s12933_024_02298_9 crossref_citationtrail_10_1186_s12933_024_02298_9 |
| ProviderPackageCode | CITATION AAYXX |
| PublicationCentury | 2000 |
| PublicationDate | 2024-06-28 |
| PublicationDateYYYYMMDD | 2024-06-28 |
| PublicationDate_xml | – month: 06 year: 2024 text: 2024-06-28 day: 28 |
| PublicationDecade | 2020 |
| PublicationPlace | England |
| PublicationPlace_xml | – name: England – name: London |
| PublicationTitle | Cardiovascular diabetology |
| PublicationTitleAlternate | Cardiovasc Diabetol |
| PublicationYear | 2024 |
| Publisher | BioMed Central BMC |
| Publisher_xml | – name: BioMed Central – name: BMC |
| References | XZ Zhang (2298_CR72) 2023; 14 T Wu (2298_CR37) 2021; 2 R Marfella (2298_CR52) 2022; 184 SD Anker (2298_CR11) 2021; 385 C Lin (2298_CR13) 2022; 24 KM Gurses (2298_CR64) 2017; 69 JJV McMurray (2298_CR10) 2019; 381 JA Requena-Ibáñez (2298_CR30) 2021; 9 LM Schriml (2298_CR43) 2019; 47 AN von Krusenstiern (2298_CR79) 2023; 19 NR Pugliese (2298_CR28) 2021; 23 TA McDonagh (2298_CR4) 2022; 75 M Brezinova (2298_CR45) 2018; 1863 2298_CR47 C Florean (2298_CR80) 2019; 134 CW Yancy (2298_CR5) 2017; 70 E Diaz-Rodriguez (2298_CR48) 2018; 114 R Marfella (2298_CR53) 2022; 127 Y Hirata (2298_CR65) 2011; 58 M Packer (2298_CR25) 2018; 71 W Miao (2298_CR86) 2022; 2022 M Ashburner (2298_CR38) 2000; 25 G Iacobellis (2298_CR20) 2022; 45 G Lippi (2298_CR2) 2020; 5 L Monzo (2298_CR50) 2021; 115 A Elsanhoury (2298_CR26) 2021; 8 T Sato (2298_CR62) 2018; 17 FJ Martin (2298_CR35) 2023; 51 AR Pico (2298_CR41) 2008; 6 AS Antonopoulos (2298_CR54) 2017; 595 A Agrawal (2298_CR42) 2024; 52 HS Sacks (2298_CR21) 2007; 153 H Kong (2298_CR81) 2020; 6 H Feng (2298_CR85) 2020; 30 D Wang (2298_CR63) 2022; 13 VA Rossi (2298_CR22) 2023; 24 AM Fratta Pasini (2298_CR88) 2023; 12 JRB Dyck (2298_CR14) 2022; 167 JS Aguilar-Gallardo (2298_CR15) 2021; 8 B Gaborit (2298_CR33) 2021; 20 KM Lauritsen (2298_CR49) 2022; 11 G Iacobellis (2298_CR31) 2020; 28 M Milacic (2298_CR40) 2024; 52 S Nishimura (2298_CR71) 2009; 15 S Yagi (2298_CR32) 2017; 9 A Sahebkar (2298_CR87) 2023; 146 TM Lee (2298_CR69) 2017; 104 M Packer (2298_CR9) 2020; 383 TM Gorter (2298_CR23) 2020; 8 V Quagliariello (2298_CR61) 2021; 20 CK Wu (2298_CR24) 2020; 22 M Barchuk (2298_CR74) 2020; 40 A Venkateshvaran (2298_CR27) 2022; 24 P Tomášová (2298_CR73) 2019; 1113 P Janovska (2298_CR76) 2020; 11 C Doesch (2298_CR29) 2010; 12 W Chen (2298_CR89) 2023; 14 S Nattel (2298_CR57) 2017; 3 SD Solomon (2298_CR12) 2022; 387 C Gene Ontology (2298_CR39) 2023; 224 M Brezinova (2298_CR44) 2020; 1865 R Lage (2298_CR55) 2015; 416 C Sardu (2298_CR70) 2023; 22 M El Hout (2298_CR84) 2018; 53 G Iacobellis (2298_CR18) 2005; 2 W Masson (2298_CR51) 2021; 10 MI Love (2298_CR36) 2014; 15 A Groenewegen (2298_CR3) 2020; 22 L Xu (2298_CR67) 2017; 20 LE Fosshaug (2298_CR59) 2015; 21 A Aragón-Herrera (2298_CR60) 2023; 161 B Neal (2298_CR8) 2017; 377 Z Pang (2298_CR46) 2021; 49 M Barchuk (2298_CR75) 2022; 42 T Skotland (2298_CR77) 2019; 10 W Mullens (2298_CR17) 2021; 9 T Mazurek (2298_CR56) 2003; 108 VB Patel (2298_CR66) 2016; 65 P Theofilis (2298_CR16) 2022; 188 Z Matloch (2298_CR19) 2016; 65 2298_CR34 B Bozkurt (2298_CR1) 2021; 23 B Zinman (2298_CR6) 2015; 373 Y Mori (2298_CR68) 2019; 18 L Zhao (2298_CR58) 2020; 24 SD Wiviott (2298_CR7) 2019; 380 R Miao (2298_CR78) 2023; 14 CF Chiu (2298_CR82) 2017; 139 M Gao (2298_CR83) 2015; 59 |
| References_xml | – volume: 416 start-page: 77 year: 2015 ident: 2298_CR55 publication-title: Mol Cell Endocrinol doi: 10.1016/j.mce.2015.08.025 – volume: 22 start-page: 1342 issue: 8 year: 2020 ident: 2298_CR3 publication-title: Eur J Heart Fail doi: 10.1002/ejhf.1858 – volume: 1865 start-page: 158576 issue: 2 year: 2020 ident: 2298_CR44 publication-title: Biochim Biophys Acta Mol Cell Biol Lipids doi: 10.1016/j.bbalip.2019.158576 – volume: 58 start-page: 248 issue: 3 year: 2011 ident: 2298_CR65 publication-title: J Am Coll Cardiol doi: 10.1016/j.jacc.2011.01.048 – volume: 383 start-page: 1413 issue: 15 year: 2020 ident: 2298_CR9 publication-title: N Engl J Med doi: 10.1056/NEJMoa2022190 – volume: 21 start-page: 916 issue: 11 year: 2015 ident: 2298_CR59 publication-title: J Card Fail doi: 10.1016/j.cardfail.2015.07.014 – volume: 10 start-page: 2150 issue: 8 year: 2021 ident: 2298_CR51 publication-title: Cells doi: 10.3390/cells10082150 – volume: 184 start-page: 106448 year: 2022 ident: 2298_CR52 publication-title: Pharmacol Res doi: 10.1016/j.phrs.2022.106448 – volume: 52 start-page: D679 issue: D1 year: 2024 ident: 2298_CR42 publication-title: Nucleic Acids Res doi: 10.1093/nar/gkad960 – volume: 15 start-page: 914 issue: 8 year: 2009 ident: 2298_CR71 publication-title: Nat Med doi: 10.1038/nm.1964 – volume: 20 start-page: 57 issue: 1 year: 2021 ident: 2298_CR33 publication-title: Cardiovasc Diabetol doi: 10.1186/s12933-021-01237-2 – volume: 14 start-page: 186 issue: 3 year: 2023 ident: 2298_CR78 publication-title: Cell Death Dis doi: 10.1038/s41419-023-05708-0 – volume: 28 start-page: 1068 issue: 6 year: 2020 ident: 2298_CR31 publication-title: Obesity doi: 10.1002/oby.22798 – volume: 65 start-page: 23 issue: 1 year: 2016 ident: 2298_CR19 publication-title: Physiol Res doi: 10.33549/physiolres.933036 – volume: 14 start-page: 1078205 year: 2023 ident: 2298_CR89 publication-title: Front Pharmacol doi: 10.3389/fphar.2023.1078205 – volume: 1863 start-page: 126 issue: 2 year: 2018 ident: 2298_CR45 publication-title: Biochim Biophys Acta Mol Cell Biol Lipids doi: 10.1016/j.bbalip.2017.11.004 – volume: 6 start-page: eabb7272 issue: 45 year: 2020 ident: 2298_CR81 publication-title: Sci Adv doi: 10.1126/sciadv.abb7272 – volume: 15 start-page: 550 issue: 12 year: 2014 ident: 2298_CR36 publication-title: Genome Biol doi: 10.1186/s13059-014-0550-8 – volume: 104 start-page: 298 year: 2017 ident: 2298_CR69 publication-title: Free Radic Biol Med doi: 10.1016/j.freeradbiomed.2017.01.035 – volume: 22 start-page: 80 issue: 1 year: 2023 ident: 2298_CR70 publication-title: Cardiovasc Diabetol doi: 10.1186/s12933-023-01814-7 – volume: 53 start-page: 125 year: 2018 ident: 2298_CR84 publication-title: Semin Cancer Biol doi: 10.1016/j.semcancer.2018.07.009 – volume: 30 start-page: 3411 issue: 10 year: 2020 ident: 2298_CR85 publication-title: Cell Rep doi: 10.1016/j.celrep.2020.02.049 – volume: 8 start-page: 720690 year: 2021 ident: 2298_CR26 publication-title: Front Cardiovasc Med doi: 10.3389/fcvm.2021.720690 – volume: 146 start-page: 155659 year: 2023 ident: 2298_CR87 publication-title: Metab Clin Exp doi: 10.1016/j.metabol.2023.155659 – volume: 13 start-page: 1045235 year: 2022 ident: 2298_CR63 publication-title: Front Pharmacol doi: 10.3389/fphar.2022.1045235 – volume: 14 start-page: 1126997 year: 2023 ident: 2298_CR72 publication-title: Front Immunol doi: 10.3389/fimmu.2023.1126997 – volume: 9 start-page: 590 issue: 8 year: 2021 ident: 2298_CR17 publication-title: JACC: Heart Fail – volume: 11 start-page: e210558 issue: 4 year: 2022 ident: 2298_CR49 publication-title: Endocr Connect doi: 10.1530/EC-21-0558 – volume: 25 start-page: 25 issue: 1 year: 2000 ident: 2298_CR38 publication-title: Nat Genet doi: 10.1038/75556 – volume: 224 start-page: iyad031 issue: 1 year: 2023 ident: 2298_CR39 publication-title: Genetics doi: 10.1093/genetics/iyad031 – volume: 188 start-page: 109927 year: 2022 ident: 2298_CR16 publication-title: Diabetes Res Clin Pract doi: 10.1016/j.diabres.2022.109927 – volume: 71 start-page: 2360 issue: 20 year: 2018 ident: 2298_CR25 publication-title: J Am Coll Cardiol doi: 10.1016/j.jacc.2018.03.509 – volume: 11 start-page: 1614 issue: 6 year: 2020 ident: 2298_CR76 publication-title: J Cachexia Sarcopenia Muscle doi: 10.1002/jcsm.12631 – volume: 49 start-page: W388 issue: W1 year: 2021 ident: 2298_CR46 publication-title: Nucleic Acids Res doi: 10.1093/nar/gkab382 – volume: 3 start-page: 425 issue: 5 year: 2017 ident: 2298_CR57 publication-title: JACC Clin Electrophysiol doi: 10.1016/j.jacep.2017.03.002 – volume: 1113 start-page: 50 year: 2019 ident: 2298_CR73 publication-title: J Chromatogr B doi: 10.1016/j.jchromb.2019.03.006 – volume: 47 start-page: D955 issue: D1 year: 2019 ident: 2298_CR43 publication-title: Nucleic Acids Res doi: 10.1093/nar/gky1032 – volume: 377 start-page: 2099 issue: 21 year: 2017 ident: 2298_CR8 publication-title: N Engl J Med – volume: 139 start-page: 4859 issue: 13 year: 2017 ident: 2298_CR82 publication-title: J Am Chem Soc doi: 10.1021/jacs.7b00390 – volume: 20 start-page: 150 issue: 1 year: 2021 ident: 2298_CR61 publication-title: Cardiovasc Diabetol doi: 10.1186/s12933-021-01346-y – volume: 127 start-page: 154936 year: 2022 ident: 2298_CR53 publication-title: Metabolism doi: 10.1016/j.metabol.2021.154936 – volume: 22 start-page: 445 issue: 3 year: 2020 ident: 2298_CR24 publication-title: Eur J Heart Fail doi: 10.1002/ejhf.1617 – volume: 24 start-page: 511 issue: 1 year: 2020 ident: 2298_CR58 publication-title: J Cell Mol Med doi: 10.1111/jcmm.14758 – volume: 18 start-page: 143 issue: 1 year: 2019 ident: 2298_CR68 publication-title: Cardiovasc Diabetol doi: 10.1186/s12933-019-0947-5 – volume: 52 start-page: D672 issue: D1 year: 2024 ident: 2298_CR40 publication-title: Nucleic Acids Res doi: 10.1093/nar/gkad1025 – volume: 373 start-page: 2117 issue: 22 year: 2015 ident: 2298_CR6 publication-title: N Engl J Med doi: 10.1056/NEJMoa1504720 – volume: 42 start-page: e242 issue: 8 year: 2022 ident: 2298_CR75 publication-title: Arterioscler Thromb Vasc Biol doi: 10.1161/ATVBAHA.122.317840 – volume: 20 start-page: 137 year: 2017 ident: 2298_CR67 publication-title: EBioMedicine doi: 10.1016/j.ebiom.2017.05.028 – volume: 19 start-page: 719 issue: 6 year: 2023 ident: 2298_CR79 publication-title: Nat Chem Biol doi: 10.1038/s41589-022-01249-3 – volume: 10 start-page: 2752 issue: 1 year: 2019 ident: 2298_CR77 publication-title: Nat Commun doi: 10.1038/s41467-019-10711-1 – volume: 24 start-page: 2251 issue: 12 year: 2022 ident: 2298_CR27 publication-title: Eur J Heart Fail doi: 10.1002/ejhf.2709 – ident: 2298_CR47 – volume: 385 start-page: 1451 issue: 16 year: 2021 ident: 2298_CR11 publication-title: N Engl J Med doi: 10.1056/NEJMoa2107038 – volume: 51 start-page: D933 issue: D1 year: 2023 ident: 2298_CR35 publication-title: Nucleic Acids Res doi: 10.1093/nar/gkac958 – volume: 380 start-page: 347 issue: 4 year: 2019 ident: 2298_CR7 publication-title: N Engl J Med doi: 10.1056/NEJMoa1812389 – volume: 161 start-page: 114535 year: 2023 ident: 2298_CR60 publication-title: Biomed Pharmacother doi: 10.1016/j.biopha.2023.114535 – volume: 6 start-page: e184 issue: 7 year: 2008 ident: 2298_CR41 publication-title: PLoS Biol doi: 10.1371/journal.pbio.0060184 – volume: 108 start-page: 2460 issue: 20 year: 2003 ident: 2298_CR56 publication-title: Circulation doi: 10.1161/01.CIR.0000099542.57313.C5 – volume: 9 start-page: 578 issue: 8 year: 2021 ident: 2298_CR30 publication-title: JACC: Heart Fail – volume: 24 start-page: 6838 issue: 7 year: 2023 ident: 2298_CR22 publication-title: Int J Mol Sci doi: 10.3390/ijms24076838 – volume: 5 start-page: 15 year: 2020 ident: 2298_CR2 publication-title: AME Med J doi: 10.21037/amj.2020.03.03 – volume: 69 start-page: 851 issue: 6 year: 2017 ident: 2298_CR64 publication-title: J Cardiol doi: 10.1016/j.jjcc.2016.08.016 – volume: 24 start-page: 550 issue: 3 year: 2022 ident: 2298_CR13 publication-title: Diabetes Obes Metab doi: 10.1111/dom.14596 – volume: 153 start-page: 907 issue: 6 year: 2007 ident: 2298_CR21 publication-title: Am Heart J doi: 10.1016/j.ahj.2007.03.019 – ident: 2298_CR34 – volume: 115 start-page: 154452 year: 2021 ident: 2298_CR50 publication-title: Metabolism doi: 10.1016/j.metabol.2020.154452 – volume: 70 start-page: 776 issue: 6 year: 2017 ident: 2298_CR5 publication-title: J Am Coll Cardiol doi: 10.1016/j.jacc.2017.04.025 – volume: 59 start-page: 298 issue: 2 year: 2015 ident: 2298_CR83 publication-title: Mol Cell doi: 10.1016/j.molcel.2015.06.011 – volume: 17 start-page: 6 issue: 1 year: 2018 ident: 2298_CR62 publication-title: Cardiovasc Diabetol doi: 10.1186/s12933-017-0658-8 – volume: 23 start-page: 1858 issue: 11 year: 2021 ident: 2298_CR28 publication-title: Eur J Heart Fail doi: 10.1002/ejhf.2337 – volume: 134 start-page: 177 year: 2019 ident: 2298_CR80 publication-title: Free Radic Biol Med doi: 10.1016/j.freeradbiomed.2019.01.008 – volume: 75 start-page: 523 issue: 6 year: 2022 ident: 2298_CR4 publication-title: Rev Esp Cardiol (Engl Ed) doi: 10.1016/j.recesp.2021.11.027 – volume: 8 start-page: 667 issue: 8 year: 2020 ident: 2298_CR23 publication-title: JACC Heart Fail doi: 10.1016/j.jchf.2020.06.003 – volume: 23 start-page: 352 issue: 3 year: 2021 ident: 2298_CR1 publication-title: Eur J Heart Fail doi: 10.1002/ejhf.2115 – volume: 595 start-page: 3907 issue: 12 year: 2017 ident: 2298_CR54 publication-title: J Physiol doi: 10.1113/JP273049 – volume: 381 start-page: 1995 issue: 21 year: 2019 ident: 2298_CR10 publication-title: N Engl J Med doi: 10.1056/NEJMoa1911303 – volume: 9 start-page: 78 issue: 1 year: 2017 ident: 2298_CR32 publication-title: Diabetol Metab Syndr doi: 10.1186/s13098-017-0275-4 – volume: 114 start-page: 336 issue: 2 year: 2018 ident: 2298_CR48 publication-title: Cardiovasc Res doi: 10.1093/cvr/cvx186 – volume: 45 start-page: 489 issue: 3 year: 2022 ident: 2298_CR20 publication-title: J Endocrinol Investig doi: 10.1007/s40618-021-01687-1 – volume: 2022 start-page: 8373389 year: 2022 ident: 2298_CR86 publication-title: Mediat Inflamm doi: 10.1155/2022/8373389 – volume: 12 start-page: 867 issue: 6 year: 2023 ident: 2298_CR88 publication-title: Cells doi: 10.3390/cells12060867 – volume: 8 start-page: 311 issue: 3 year: 2021 ident: 2298_CR15 publication-title: Eur Heart J Cardiovasc Pharmacother doi: 10.1093/ehjcvp/pvab056 – volume: 40 start-page: 986 issue: 4 year: 2020 ident: 2298_CR74 publication-title: Arterioscler Thromb Vasc Biol doi: 10.1161/ATVBAHA.120.313955 – volume: 2 start-page: 536 issue: 10 year: 2005 ident: 2298_CR18 publication-title: Nat Clin Pract Cardiovasc Med doi: 10.1038/ncpcardio0319 – volume: 387 start-page: 1089 issue: 12 year: 2022 ident: 2298_CR12 publication-title: N Engl J Med doi: 10.1056/NEJMoa2206286 – volume: 167 start-page: 17 year: 2022 ident: 2298_CR14 publication-title: J Mol Cell Cardiol doi: 10.1016/j.yjmcc.2022.03.005 – volume: 12 start-page: 40 issue: 1 year: 2010 ident: 2298_CR29 publication-title: J Cardiovasc Magn Reson doi: 10.1186/1532-429X-12-40 – volume: 2 start-page: 100141 issue: 3 year: 2021 ident: 2298_CR37 publication-title: Innovation (Cambridge) – volume: 65 start-page: 85 issue: 1 year: 2016 ident: 2298_CR66 publication-title: Diabetes doi: 10.2337/db15-0399 |
| SSID | ssj0017861 |
| Score | 2.4251075 |
| Snippet | Sodium-glucose cotransporter 2 inhibitors (SGLT-2i) are glucose-lowering agents used for the treatment of type 2 diabetes mellitus, which also improve heart... BackgroundSodium-glucose cotransporter 2 inhibitors (SGLT-2i) are glucose-lowering agents used for the treatment of type 2 diabetes mellitus, which also... Abstract Background Sodium-glucose cotransporter 2 inhibitors (SGLT-2i) are glucose-lowering agents used for the treatment of type 2 diabetes mellitus, which... |
| SourceID | doaj proquest pubmed crossref |
| SourceType | Open Website Aggregation Database Index Database Enrichment Source |
| StartPage | 223 |
| SubjectTerms | Adipose tissue Adipose Tissue - drug effects Adipose Tissue - metabolism Anti-Inflammatory Agents - pharmacology Anti-Inflammatory Agents - therapeutic use Architects Biomarkers - blood Body fat Body mass index Cardiovascular disease Cardiovascular diseases Congestive heart failure Coronary vessels Cytokines Data analysis Diabetes Diabetes mellitus (non-insulin dependent) Diabetes Mellitus, Type 2 - diagnosis Diabetes Mellitus, Type 2 - drug therapy Diabetes Mellitus, Type 2 - metabolism Ejection fraction Epicardial Adipose Tissue Ether lipids Female Ferroptosis Flow cytometry Gene expression Glucose Health risks Heart diseases Heart failure Heart Failure - drug therapy Heart Failure - metabolism Heart Failure - physiopathology Heart transplantation Heart transplants Humans Inflammation Inflammation Mediators - metabolism Lipid metabolism Lymphocytes Male Metabolomics Middle Aged Mortality Obesity Oleic acid Oxidative stress Patients Pericardium - drug effects Pericardium - metabolism Severity of Illness Index Sodium Sodium-glucose cotransporter Sodium-glucose cotransporter 2 inhibitors Sodium-Glucose Transporter 2 Inhibitors - adverse effects Sodium-Glucose Transporter 2 Inhibitors - pharmacology Sodium-Glucose Transporter 2 Inhibitors - therapeutic use Stroke Volume - drug effects Treatment Outcome Ventricular Function, Left - drug effects |
| SummonAdditionalLinks | – databaseName: DOAJ Directory of Open Access Journals dbid: DOA link: http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwrV3Lat0wEBUli9BNadOX06So0F0xuVcPW1q2ISEU0k0byE7oNcSQ2Bfb93_6qR3JD9pF200WBiNLSOic0Yw08gwhH50AHlBPlaCdLUU9-Xc3pY4oWAFY8C55dK-_VVc34uutvP0t1Ve6EzaFB54m7gykq5123toohA1ogQPXQoHjKRRVcGn1RZ23bKZm_0Gtqu3yi4yqzoak1ZK_UuDDNIr4H2ooR-v_u4mZVc3lc_JsthHp52lsL8iT2B6Rw-vZC_6S_PzehWb_sFw3p74b1xDlPWW0ae8a16Q0OvgaEDuK09eUyCWE_yG71bEkTKUQ-77bjR32RYe7BkZsQ-MOsUvUuac2NLvUyZgRoh3QYe_S4c1A0xkuRc0a-0hTYuyRgm3SNfdX5Oby4sf5VTlnWig9mkNjCRsftbIMlLCoxIPSEQSih8WcgwVebSuvwUsp6yAFbFylgFlZAxrnwCJ_TQ7aro1vCY08WolYRVt75IHUuGo4CDaosAksxoJsl4k3fg5DnrJh3Ju8HVGVmcAyCJbJYBldkE9rm90UhOOftb8kPNeaKYB2LkBamZlW5n-0KsjJwgYzS_VgcD3UDPU5UwX5sH5GeUxOFtvGbp_r8HqLZmZdkDcTi9aR8BTsHne0x48xwnfkKcuErkqmTsjB2O_jKRpIo3ufZeEX7XcSZA priority: 102 providerName: Directory of Open Access Journals – databaseName: Health & Medical Collection dbid: 7X7 link: http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwfV1Ni9YwEA66gngRv7e6SgRvUvZtmrbJSVRcFmG96MJ7K_kat7Db1rbv__GnOpN-iAf3UChp2oQ8z2QmmXSGsXdWQu5RT6WgrUllNft3d6kOKFgehHeWPLoX38rzS_l1X-yXDbdxOVa5zolxovadoz3yU-SiFjiXCvWh_5VS1ijyri4pNO6yexS6jI50VfttwZVVqszWH2VUeTqSbiOvpcRLaBT0f5RRjNn_f0MzKpyzR-zhYinyjzO0j9md0D5h9y8WX_hT9vt755vDzXronLtu2gKVD1zwpr1qbEPJdPDWI4IcB7FJkVFIgpvoXMcSP5dCGIaunzpsi49XDUz4Dg89IkgEuubGNz01MkWceAd8PFjawhk57eRy1K9hCJzSY08cTEOH3Z-xy7MvPz6fp0u-hdShUTSlsHNBKyNASYOq3CsdQCKGWJznYCAvs9JpcEVRVL6QsLOlAmGKCtBEBxHy5-yo7dpwzHjIgylMkMFUDtlQaJw7LHjjld95EULCsnXga7cEI6ecGNd1XJSosp7BqhGsOoJV64S9397p51Act9b-RHhuNSmMdizohp_1IpU1FLay2jqDXZXG4_IOci0V2JzinHmbsJOVDfUi22P9l4kJe7s9RqkkV4tpQ3eIdfIqQ2OzStiLmUVbT3IKeY_r2pe3f_wVeyAiVctUqBN2NA2H8BoNoMm-iSz_A71PCKc priority: 102 providerName: ProQuest |
| Title | Sodium-glucose cotransporter 2 inhibitors induce anti-inflammatory and anti-ferroptotic shift in epicardial adipose tissue of subjects with severe heart failure |
| URI | https://www.ncbi.nlm.nih.gov/pubmed/38943140 https://www.proquest.com/docview/3079228428 https://www.proquest.com/docview/3073712647 https://doaj.org/article/f5b7b9bcaae44ad086f3948fb34547db |
| Volume | 23 |
| hasFullText | 1 |
| inHoldings | 1 |
| isFullTextHit | |
| isPrint | |
| link | http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwlV3di9QwEA_3AeKL-G31XCL4JtXdJmmaBxFP7jiEPURd2LeSNJm7wl67tl24-2_8U52kHyKcgg-FkqZNmt9vMpNMO0PIa8OBWdRTMSijYy57_-48Vg4Fy0JiC-M9usvz9GzFP6_Feo-M6Y6GAWxvXdr5fFKrZvP2-sfNBxT490Hgs_Rd63WW90ZyPBKFArxPDlEzSS-oS_7bqyCzPn4qlyLGaXk-_kRz6zP-UFQhnv_fjdCgjE7vk3uDFUk_9rA_IHuuekjuLAc_-SPy81tty93V-EE6LepuCmLe0ISW1WVpSp9oB08toktxgMsY3x8JchUc71hi-1JwTVNvuxrbou1lCR3eQ90W0fXk2lBty61vpAsY0hpouzN-e6elfpeXou51jaM-dXZHQZf-Q_jHZHV68v3TWTzkYogLNJi6GOaFU5lOIOMa1bzNlAOO-GIxY6CBpYu0UFAIIaQVHOYmzSDRQgKa75A49oQcVHXlnhHqmNNCO-60LJApQuG8YsBqm9m5TZyLyGIc-LwYApX7fBmbPCxYsjTvwcoRrDyAlauIvJnu2fZhOv5Z-9jjOdX0IbZDQd1c5IPE5iCMNMoUGrvKtcWlHzDFMzDMx0CzJiJHIxvykbY5zpgqQWolWUReTZdRYr0bRleu3oU6TC7QEJURedqzaOoJ8-Hwcc37_L_e5wW5mwTmpkjrI3LQNTv3Em2lzszIvlzLGTk8Pjn_8nUWdhxmQSh-AZ75FPY |
| linkProvider | Scholars Portal |
| linkToHtml | http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwtV1Lb9QwELbKVoJeEG8WChgJTijqru0k9gEhCq22tLtC0Eq9GTv20EjtZptkhfg3_AJ-I-O8EAd66yFS5PilzOd5eOwZQl5ZAdyhnIpAWROJtPXvTiLlcWE5YC6zwaM7XySzE_HpND7dIL_7uzDhWGXPExtG7Yos7JHvIBYVQ17K5LvVZRSyRgXvap9Co4XFof_5A0226u3BR6Tva8b2944_zKIuq0CUoeivI5hkXknDQAqDAstJ5UHgTLGYczDAk2mSKcjiOE5dLGBiEwnMxCmgIgrMc-z3BtkUHE2ZEdnc3Vt8_jL4LVKZTPurOTLZqYI0DX5SgQ9TyFr-EX9NloD_q7aNiNu_Q253uil934LpLtnwy3vk5rzzvt8nv74WLl9f9MfcaVbUQ2j0kjKaL89ym4f0PfjqEDMUyZZHiGGE3UXjzscS15aCL8tiVRc4Fq3OcqixDfUrxEyA7Dk1Ll-FQeoGGbQAWq1t2DSqaNg7pijRfelpSMhdUzB5OF7_gJxcCy0ektGyWPrHhHruTWy88CbNEH-xQm5lwRkn3cQx78dk2v94nXXhz0MWjnPdmEEy0S2xNBJLN8TSakzeDG1WbfCPK2vvBnoONUPg7qagKL_rjg9oiG1qlc0MTlUYhwYlcCUkWB4iqzk7Jts9GnTHTSr9F_tj8nL4jHwgOHfM0hfrpg5Pp6jepmPyqEXRMBMeguyjJf3k6s5fkFuz4_mRPjpYHD4lW6yBbRIxuU1Gdbn2z1D9qu3zDvOUfLvuZfYHmUlH_A |
| openUrl | ctx_ver=Z39.88-2004&ctx_enc=info%3Aofi%2Fenc%3AUTF-8&rfr_id=info%3Asid%2Fsummon.serialssolutions.com&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.atitle=Sodium-glucose+cotransporter+2+inhibitors+induce+anti-inflammatory+and+anti-ferroptotic+shift+in+epicardial+adipose+tissue+of+subjects+with+severe+heart+failure&rft.jtitle=Cardiovascular+diabetology&rft.au=Kasperova%2C+Barbora+Judita&rft.au=Mraz%2C+Milos&rft.au=Svoboda%2C+Petr&rft.au=Hlavacek%2C+Daniel&rft.date=2024-06-28&rft.issn=1475-2840&rft.eissn=1475-2840&rft.volume=23&rft.issue=1&rft_id=info:doi/10.1186%2Fs12933-024-02298-9&rft.externalDBID=n%2Fa&rft.externalDocID=10_1186_s12933_024_02298_9 |
| thumbnail_l | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/lc.gif&issn=1475-2840&client=summon |
| thumbnail_m | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/mc.gif&issn=1475-2840&client=summon |
| thumbnail_s | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/sc.gif&issn=1475-2840&client=summon |