<?xml version="1.0" encoding="UTF-8"?>
<!DOCTYPE root>
<article xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xmlns:ali="http://www.niso.org/schemas/ali/1.0/" article-type="review-article" dtd-version="1.2" xml:lang="en"><front><journal-meta><journal-id journal-id-type="publisher-id">Perm Medical Journal</journal-id><journal-title-group><journal-title xml:lang="en">Perm Medical Journal</journal-title><trans-title-group xml:lang="ru"><trans-title>Пермский медицинский журнал (сетевое издание "Perm medical journal")</trans-title></trans-title-group></journal-title-group><issn publication-format="print">0136-1449</issn><issn publication-format="electronic">2687-1408</issn><publisher><publisher-name xml:lang="en">Eco-Vector</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="publisher-id">633386</article-id><article-id pub-id-type="doi">10.17816/pmj41692-108</article-id><article-categories><subj-group subj-group-type="toc-heading" xml:lang="en"><subject>Literature review</subject></subj-group><subj-group subj-group-type="toc-heading" xml:lang="ru"><subject>Обзор литературы</subject></subj-group><subj-group subj-group-type="article-type"><subject>Review Article</subject></subj-group></article-categories><title-group><article-title xml:lang="en">Contemporary prospects for the use of sodium-glucose cotransporter-2 inhibitors</article-title><trans-title-group xml:lang="ru"><trans-title>Современные перспективы применения препаратов группы ингибиторов натрий-глюкозного котранспортера 2-го типа</trans-title></trans-title-group></title-group><contrib-group><contrib contrib-type="author"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0001-8450-4537</contrib-id><name-alternatives><name xml:lang="en"><surname>Kondratieva</surname><given-names>A. R.</given-names></name><name xml:lang="ru"><surname>Кондратьева</surname><given-names>А. Р.</given-names></name></name-alternatives><address><country country="RU">Russian Federation</country></address><bio xml:lang="en"><p>5<sup>th</sup>-year Student of the Medical Faculty</p></bio><bio xml:lang="ru"><p>студент V курса лечебного факультета</p></bio><email>zwx2@mail.ru</email><xref ref-type="aff" rid="aff1"/></contrib><contrib contrib-type="author"><contrib-id contrib-id-type="orcid">https://orcid.org/0009-0001-0962-8668</contrib-id><name-alternatives><name xml:lang="en"><surname>Khazova</surname><given-names>E. A.</given-names></name><name xml:lang="ru"><surname>Хазова</surname><given-names>Е. А.</given-names></name></name-alternatives><address><country country="RU">Russian Federation</country></address><bio xml:lang="en"><p>5<sup>th</sup>-year Student of the Medical Faculty</p></bio><bio xml:lang="ru"><p>студент V курса лечебного факультета</p></bio><email>zwx2@mail.ru</email><xref ref-type="aff" rid="aff1"/></contrib><contrib contrib-type="author"><contrib-id contrib-id-type="orcid">https://orcid.org/0009-0008-5012-3312</contrib-id><name-alternatives><name xml:lang="en"><surname>Lobanova</surname><given-names>A. V.</given-names></name><name xml:lang="ru"><surname>Лобанова</surname><given-names>А. В.</given-names></name></name-alternatives><address><country country="RU">Russian Federation</country></address><bio xml:lang="en"><p>5<sup>th</sup>-year of the Medical Faculty</p></bio><bio xml:lang="ru"><p>студент V курса лечебного факультета</p></bio><email>zwx2@mail.ru</email><xref ref-type="aff" rid="aff1"/></contrib><contrib contrib-type="author"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0001-8430-237X</contrib-id><name-alternatives><name xml:lang="en"><surname>Sorokina</surname><given-names>Yu. A.</given-names></name><name xml:lang="ru"><surname>Сорокина</surname><given-names>Ю. А.</given-names></name></name-alternatives><address><country country="RU">Russian Federation</country></address><bio xml:lang="en"><p>PhD (Biology), Associate Professor of the Department of General and Clinical Pharmacology</p></bio><bio xml:lang="ru"><p>доцент кафедры общей и клинической фармакологии, кандидат биологических наук, доцент</p></bio><email>zwx2@mail.ru</email><xref ref-type="aff" rid="aff1"/></contrib><contrib contrib-type="author"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0003-3659-3576</contrib-id><name-alternatives><name xml:lang="en"><surname>Mosina</surname><given-names>A. A.</given-names></name><name xml:lang="ru"><surname>Мосина</surname><given-names>А. А.</given-names></name></name-alternatives><address><country country="RU">Russian Federation</country></address><bio xml:lang="en"><p>PhD (Biology), Assistant of the Department of General and Clinical Pharmacology</p></bio><bio xml:lang="ru"><p>асситент кафедры общей и клинической фармакологии</p></bio><email>zwx2@mail.ru</email><xref ref-type="aff" rid="aff1"/></contrib><contrib contrib-type="author"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0003-1830-3600</contrib-id><name-alternatives><name xml:lang="en"><surname>Zanozina</surname><given-names>O. V.</given-names></name><name xml:lang="ru"><surname>Занозина</surname><given-names>О. В.</given-names></name></name-alternatives><address><country country="RU">Russian Federation</country></address><bio xml:lang="en"><p>DSc (Medicine), Associate Professor, Professor of the Department of Hospital Therapy and General Medical Practice named after V.G. Vogralik, Head of the Endocrinological Department</p></bio><bio xml:lang="ru"><p>доктор медицинских наук, доцент, профессор кафедры госпитальной терапии и общей врачебной практики имени В.Г. Вогралика, заведующая эндокринологическим отделением</p></bio><email>zwx2@mail.ru</email><xref ref-type="aff" rid="aff1"/><xref ref-type="aff" rid="aff2"/></contrib></contrib-group><aff-alternatives id="aff1"><aff><institution xml:lang="en">Privolzhsky Research Medical University</institution></aff><aff><institution xml:lang="ru">Приволжский исследовательский медицинский университет</institution></aff></aff-alternatives><aff-alternatives id="aff2"><aff><institution xml:lang="en">Nizhny Novgorod Regional Clinical Hospital named after N.A. Semashko</institution></aff><aff><institution xml:lang="ru">Нижегородская областная клиническая больница имени Н.А. Семашко</institution></aff></aff-alternatives><pub-date date-type="pub" iso-8601-date="2024-12-15" publication-format="electronic"><day>15</day><month>12</month><year>2024</year></pub-date><volume>41</volume><issue>6</issue><issue-title xml:lang="en"/><issue-title xml:lang="ru"/><fpage>92</fpage><lpage>108</lpage><history><date date-type="received" iso-8601-date="2024-06-10"><day>10</day><month>06</month><year>2024</year></date></history><permissions><copyright-statement xml:lang="en">Copyright ©; 2024, Eco-Vector</copyright-statement><copyright-statement xml:lang="ru">Copyright ©; 2024, Эко-Вектор</copyright-statement><copyright-year>2024</copyright-year><copyright-holder xml:lang="en">Eco-Vector</copyright-holder><copyright-holder xml:lang="ru">Эко-Вектор</copyright-holder><ali:free_to_read xmlns:ali="http://www.niso.org/schemas/ali/1.0/"/></permissions><self-uri xlink:href="https://permmedjournal.ru/PMJ/article/view/633386">https://permmedjournal.ru/PMJ/article/view/633386</self-uri><abstract xml:lang="en"><p>To determine contemporary prospects for the use of non-glycemic effects of sodium-glucose cotransporter-2 inhibitors in comorbid patients, the analysis of existing studies was carried out.</p> <p>The mechanisms of action of sodium-glucose cotransporter-2 inhibitors discovered during the EMPA-REG OUTCOME study which were previously unknown, encouraged further research on the use of these drugs in other pathological conditions. The authors of the article have analyzed some clinical and preclinical studies on the use of this drug group in such conditions as stroke, cancer, rheumatological diseases, and rhythm disorders, as well as their impact on the development of major adverse cardiovascular events. The effects of oxidative stress suppression in the myocardium and nervous tissue with an increase in the number of mitochondria which reduces the risk of developing rhythm disorders, improves neoangiogenesis in the focus of ischemic necrosis, and has neuroprotective effects are described in the article. In oncological diseases, gliflozins prevent proliferation of tumor cells and oncogenesis through the induction of late apoptosis and also have cardioprotective effects in patients undergoing chemotherapy. The use of these medicines reduces the incidence of major adverse cardiovascular events, as well as restenosis after intravascular interventions. The positive effect on the course of rheumatological diseases was in improving laboratory parameters in a number of diseases and reducing the frequency of exacerbations and visits to a doctor in patients with gout.</p> <p>With a constant increase in the number of patients with comorbid conditions, it is important to carry out further study of pleiotropic effects of sodium-glucose cotransporter-2 inhibitors for the subsequent introduction of new data into clinical practice.</p></abstract><trans-abstract xml:lang="ru"><p>Осуществлен<bold> </bold>анализ исследований негликемических эффектов препаратов группы ингибиторов натрий-глюкозного котранспортера 2-го типа для определения современных перспектив применения данной группы лекарственных средств у коморбидных пациентов.</p> <p>Открытие в ходе исследования EMPA-REG OUTCOME неизвестных ранее механизмов действия ингибиторов натрий-глюкозного котранспортера 2-го типа дало толчок к исследованиям по применению данных препаратов и при других патологических состояниях. В связи с этим проанализированы клинические и доклинические исследования применения данной группы препаратов при таких состояниях, как инсульт, онкологические заболевания, ревматологические заболевания, нарушения ритма, а также данные, касающиеся их влияния на развитие больших неблагоприятных сердечно-сосудистых событий. Описываются эффекты подавления окислительного стресса в миокарде и нервной ткани при увеличении количества митохондрий, что приводит к снижению риска развития нарушений ритма, улучшению неоангиогенеза в очаге ишемического некроза, нейропротективным эффектам. При онкологических заболеваниях глифлозины препятствуют пролиферации опухолевых клеток и онкогенезу посредством индукции позднего апоптоза, а также обладают кардиопротективными эффектами у пациентов, получающих химиотерапию. Применение данных препаратов уменьшает частоту больших неблагоприятных сердечно-сосудистых событий, а также рестенозов после внутрисосудистых вмешательств. Показано положительное влияние на течение ревматологических заболеваний в виде улучшения лабораторных показателей при ряде заболеваний и снижения частоты обострений и обращений при подагре.</p> <p>В условиях постоянного увеличения количества пациентов с коморбидными состояниями важно дальнейшее изучение плейотропных эффектов ингибиторов натрий-глюкозного котранспортера 2-го типа для последующего внедрения новых данных в клиническую практику.</p></trans-abstract><kwd-group xml:lang="en"><kwd>Sodium-glucose cotransporter 2 inhibitors</kwd><kwd>type 2 diabetes mellitus</kwd><kwd>stroke</kwd><kwd>oncology</kwd><kwd>cardioprotection</kwd><kwd>coronary heart disease</kwd><kwd>percutaneous intervention</kwd><kwd>restenosis</kwd><kwd>rhythm disorders</kwd><kwd>atrial fibrillation</kwd></kwd-group><kwd-group xml:lang="ru"><kwd>ингибиторы натрий-глюкозного котранспортера 2-го типа</kwd><kwd>сахарный диабет 2-го типа</kwd><kwd>инсульт</kwd><kwd>онкология</kwd><kwd>кардиопротекция</kwd><kwd>ишемическая болезнь сердца</kwd><kwd>чрескожное вмешательство</kwd><kwd>рестеноз</kwd><kwd>нарушения ритма</kwd><kwd>фибрилляция предсердий</kwd></kwd-group><funding-group/></article-meta></front><body></body><back><ref-list><ref id="B1"><label>1.</label><mixed-citation>Nauck M.A. Update on developments with SGLT2 inhibitors in the management of type 2 diabetes. Drug Des Devel Ther. 2014; 8: 1335–80. DOI: 10.2147/DDDT.S50773</mixed-citation></ref><ref id="B2"><label>2.</label><mixed-citation>Cowie M.R., Fisher M. SGLT2 inhibitors: mechanisms of cardiovascular benefit beyond glycaemic control. Nat Rev Cardiol. 2020; 17 (12): 761–772. DOI: 10.1038/s41569-020-0406-8</mixed-citation></ref><ref id="B3"><label>3.</label><mixed-citation>Zinman B., Wanner C., Lachin J.M., Fitchett D., Bluhmki E., Hantel S., Mattheus M., Devins T., Johansen O.E., Woerle H.J., Broedl U.C., Inzucchi S.E.; EMPA-REG OUTCOME Investigators. Empagliflozin, Cardiovascular Outcomes, and Mortality in Type 2 Diabetes. N Engl J Med. 2015; 373 (22): 2117–28. DOI: 10.1056/NEJMoa1504720</mixed-citation></ref><ref id="B4"><label>4.</label><mixed-citation>Timmis A., Vardas P., Townsend N., Torbica A., Katus H., De Smedt D., Gale C.P., Maggioni A.P., Petersen S.E., Huculeci R., Kazakiewicz D., de Benito Rubio V., Ignatiuk B., Raisi-Estabragh Z., Pawlak A., Karagiannidis E., Treskes R., Gaita D., Beltrame J.F., McConnachie A., Bardinet I., Graham I., Flather M., Elliott P., Mossialos E.A., Weidinger F., Achenbach S.; Atlas Writing Group, European Society of Cardiology. European Society of Cardiology: cardiovascular disease statistics 2021. Eur Heart J. 2022; 43 (8): 716–799. DOI: 10.1093/eurheartj/ ehab892</mixed-citation></ref><ref id="B5"><label>5.</label><mixed-citation>Shukla V., Shakya A.K., Perez-Pinzon M.A., Dave K.R. Cerebral ischemic damage in diabetes: an inflammatory perspective. J Neuroinflammation. 2017; 14 (1): 21. DOI: 10.1186/ s12974-016-0774-5</mixed-citation></ref><ref id="B6"><label>6.</label><mixed-citation>Shim B., Stokum J.A., Moyer M., Tsymbalyuk N., Tsymbalyuk O., Keledjian K., Ivanova S., Tosun C., Gerzanich V., Simard J.M. Canagliflozin, an Inhibitor of the Na+ -Coupled D-Glucose Cotransporter, SGLT2, Inhibits Astrocyte Swelling and Brain Swelling in Cerebral Ischemia. Cells 2023; 12: 2221. DOI: 10.3390/cells12182221</mixed-citation></ref><ref id="B7"><label>7.</label><mixed-citation>Andreadou I., Efentakis P., Balafas E., Togliatto G., Davos C.H., Varela A., Dimitriou C.A., Nikolaou P.E., Maratou E., Lambadiari V., Ikonomidis I., Kostomitsopoulos N., Brizzi M.F., Dimitriadis G., Iliodromitis E.K. Empagliflozin Limits Myocardial Infarction in Vivo and Cell Death in Vitro: Role of STAT3, Mitochondria, and Redox Aspects. Front Physiol. 2017; 8: 1077. DOI: 10.3389/fphys.2017.01077</mixed-citation></ref><ref id="B8"><label>8.</label><mixed-citation>Abdel-Latif R.G., Rifaai R.A., Amin E.F. Empagliflozin alleviates neuronal apoptosis induced by cerebral ischemia/reperfusion injury through HIF-1/VEGF signaling pathway. Arch Pharm Res. 2020; 43 (5): 514–525. DOI: 10.1007/s12272-020-01237-y</mixed-citation></ref><ref id="B9"><label>9.</label><mixed-citation>Amin E.F., Rifaai R.A., Abdel-Latif R.G. Empagliflozin attenuates transient cerebral ischemia/reperfusion injury in hyperglycemic rats via repressing oxidative-inflammatory-apoptotic pathway. Fundam Clin Pharmacol. 2020; 34 (5): 548–558. DOI: 10.1111/fcp.12548</mixed-citation></ref><ref id="B10"><label>10.</label><mixed-citation>Hayden M.R., Grant D.G., Aroor A.R., DeMarco V.G. Empagliflozin Ameliorates Type 2 Diabetes-Induced Ultrastructural Remodeling of the Neurovascular Unit and Neuroglia in the Female db/db Mouse. Brain Sci. 2019; 9 (3): 57. DOI: 10.3390/brainsci9030057</mixed-citation></ref><ref id="B11"><label>11.</label><mixed-citation>Vercalsteren E., Karampatsi D., Buizza C., Nyström T., Klein T., Paul G., Patrone C., Darsalia V. The SGLT2 inhibitor Empagliflozin promotes post-stroke functional recovery in diabetic mice. Cardiovasc Diabetol. 2024; 23 (1): 88. DOI: 10.1186/ s12933-024-02174-6</mixed-citation></ref><ref id="B12"><label>12.</label><mixed-citation>Vercalsteren E., Karampatsi D., Buizza C., Nyström T., Klein T., Paul G., Patrone C., Darsalia V. The SGLT2 inhibitor Empagliflozin promotes post-stroke functional recovery in diabetic mice. Cardiovasc Diabetol. 2024; 23 (1): 88. DOI: 10.1186/s12933-024-02174-6</mixed-citation></ref><ref id="B13"><label>13.</label><mixed-citation>Jiang Y., Han J., Li Y., Wu Y., Liu N., Shi S.X., Lin L., Yuan J., Wang S., Ning M.M., Dumont A.S., Wang X. Delayed rFGF21 Administration Improves Cerebrovascular Remodeling and White Matter Repair After Focal Stroke in Diabetic Mice. Transl Stroke Res. 2022; 13 (2): 311–325. DOI: 10.1007/s12975-021-00941-1</mixed-citation></ref><ref id="B14"><label>14.</label><mixed-citation>Dordoe C., Chen K., Huang W., Chen J., Hu J., Wang X., Lin L. Roles of Fibroblast Growth Factors and Their Therapeutic Potential in Treatment of Ischemic Stroke. Front Pharmacol. 2021; 12: 671131. DOI: 10.3389/fphar.2021.671131</mixed-citation></ref><ref id="B15"><label>15.</label><mixed-citation>Jiang Y., Liu N., Wang Q., Yu Z., Lin L., Yuan J., Guo S., Ahn B.J., Wang X.J., Li X., Lo E.H., Sun X., Wang X. Endocrine Regulator rFGF21 (Recombinant Human Fibroblast Growth Factor 21) Improves Neurological Outcomes Following Focal Ischemic Stroke of Type 2 Diabetes Mellitus Male Mice. Stroke. 2018; 49 (12): 3039–3049. DOI: 10.1161/STROKEAHA. 118.022119</mixed-citation></ref><ref id="B16"><label>16.</label><mixed-citation>Flippo K.H., Potthoff M.J. Metabolic Messengers: FGF21. Nat Metab. 2021; 3 (3): 309–317. DOI: 10.1038/s42255-021-00354-2</mixed-citation></ref><ref id="B17"><label>17.</label><mixed-citation>Wang Z., Leng Y., Wang J., Liao H.M., Bergman J., Leeds P., Kozikowski A., Chuang D.M. Tubastatin A, an HDAC6 inhibitor, alleviates stroke-induced brain infarction and functional deficits: potential roles of -tubulin acetylation and FGF-21 up-regulation. Sci Rep. 2016; 6: 19626. DOI: 10.1038/srep19626</mixed-citation></ref><ref id="B18"><label>18.</label><mixed-citation>Gough S.M, Casella A., Ortega K.J., Hackam A.S. Neuroprotection by the Ketogenic Diet: Evidence and Controversies. Front Nutr. 2021; 8: 782657. DOI: 10.3389/fnut.2021.782657</mixed-citation></ref><ref id="B19"><label>19.</label><mixed-citation>Gibson C.L., Murphy A.N., Murphy S.P. Stroke outcome in the ketogenic state--a systematic review of the animal data. J Neurochem. 2012; 123 Suppl 2 (0 2): 52–7. DOI: 10.1111/j.1471-4159.2012.07943.x</mixed-citation></ref><ref id="B20"><label>20.</label><mixed-citation>Takashima M., Nakamura K., Kiyohara T., Wakisaka Y., Hidaka M., Takaki H., Yamanaka K., Shibahara T., Wakisaka M., Ago T., Kitazono T. Low-dose sodium-glucose cotransporter 2 inhibitor ameliorates ischemic brain injury in mice through pericyte protection without glucose-lowering effects. Commun Biol. 2022; 5 (1): 653. DOI: 10.1038/s42003-022-03605-4</mixed-citation></ref><ref id="B21"><label>21.</label><mixed-citation>Oh C.M., Cho S., Jang J.Y., Kim H., Chun S., Choi M., Park S., Ko Y.G. Cardioprotective Potential of an SGLT2 Inhibitor Against Doxorubicin-Induced Heart Failure. Korean Circ J. 2019; 49 (12): 1183–1195. DOI: 10.4070/kcj.2019.0180</mixed-citation></ref><ref id="B22"><label>22.</label><mixed-citation>Chen M. Empagliflozin attenuates doxorubicin-induced cardiotoxicity by activating AMPK/SIRT-1/PGC-1-mediated mitochondrial biogenesis. Toxicol Res (Camb). 2023; 12 (2): 216–223. DOI: 10.1093/toxres/tfad007</mixed-citation></ref><ref id="B23"><label>23.</label><mixed-citation>Quagliariello V., De Laurentiis M., Rea D., Barbieri A., Monti M.G., Carbone A., Paccone A., Altucci L., Conte M., Canale M.L., Botti G., Maurea N. The SGLT-2 inhibitor empagliflozin improves myocardial strain, reduces cardiac fibrosis and pro-inflammatory cytokines in non-diabetic mice treated with doxorubicin. Cardiovasc Diabetol. 2021; 20 (1): 150. DOI: 10.1186/s12933-021-01346-y</mixed-citation></ref><ref id="B24"><label>24.</label><mixed-citation>Barış V.Ö., Dinçsoy A.B., Gedikli E., Zırh S., Müftüoğlu S., Erdem A. Empagliflozin Significantly Prevents the Doxorubicin-induced Acute Cardiotoxicity via Non-antioxidant Pathways. Cardiovasc Toxicol. 2021; 21 (9): 747–758. DOI: 10.1007/s12012-021-09665-y</mixed-citation></ref><ref id="B25"><label>25.</label><mixed-citation>Dabour M.S., George M.Y., Daniel M.R., Blaes A.H., Zordoky B.N. The Cardioprotective and Anticancer Effects of SGLT2 Inhibitors: JACC: CardioOncology State-of-the-Art Review. JACC CardioOncol. 2024; 6 (2): 159–182. DOI: 10.1016/j.jaccao.2024.01.007</mixed-citation></ref><ref id="B26"><label>26.</label><mixed-citation>Liu Y., Wei X., Wu M., Xu J., Xu B., Kang L. Cardioprotective Roles of -Hydroxybutyrate Against Doxorubicin Induced Cardiotoxicity. Front Pharmacol. 2021; 11: 603596. DOI: 10.3389/fphar.2020.603596</mixed-citation></ref><ref id="B27"><label>27.</label><mixed-citation>Wang C.Y., Chen C.C., Lin M.H., Su H.T., Ho M.Y., Yeh J.K., Tsai M.L., Hsieh I.C., Wen M.S. TLR9 Binding to Beclin 1 and Mitochondrial SIRT3 by a Sodium-Glucose Co-Transporter 2 Inhibitor Protects the Heart from Doxorubicin Toxicity. Biology (Basel). 2020; 9 (11): 369. DOI: 10.3390/biology9110369</mixed-citation></ref><ref id="B28"><label>28.</label><mixed-citation>Tran S., Fairlie W.D., Lee E.F. BECLIN1: Protein Structure, Function and Regulation. Cells. 2021; 10 (6): 1522. DOI: 10.3390/ cells10061522</mixed-citation></ref><ref id="B29"><label>29.</label><mixed-citation>Karapetyan L., Luke J.J., Davar D. Toll-Like Receptor 9 Agonists in Cancer. Onco Targets Ther. 2020; 13: 10039–10060. DOI: 10.2147/OTT.S247050</mixed-citation></ref><ref id="B30"><label>30.</label><mixed-citation>Chen J., Chen S., Zhang B., Liu J. SIRT3 as a potential therapeutic target for heart failure. Pharmacol Res. 2021; 165: 105432. DOI: 10.1016/j.phrs.2021.105432</mixed-citation></ref><ref id="B31"><label>31.</label><mixed-citation>Abdel-Qadir H., Carrasco R., Austin P.C., Chen Y., Zhou L., Fang J., Su H.M.H., Lega I.C., Kaul P., Neilan T.G., Thavendiranathan P. The Association of Sodium-Glucose Cotransporter 2 Inhibitors With Cardiovascular Outcomes in Anthracycline-Treated Patients With Cancer. JACC CardioOncol. 2023; 5 (3): 318–328. DOI: 10.1016/j.jaccao.2023.03.011</mixed-citation></ref><ref id="B32"><label>32.</label><mixed-citation>Nakachi S., Okamoto S., Tamaki K., Nomura I., Tomihama M., Nishi Y., Fukushima T., Tanaka Y., Morishima S., Imamura M., Maeda S., Tsutsui M., Matsushita M., Masuzaki H. Impact of anti-diabetic sodium-glucose cotransporter 2 inhibitors on tumor growth of intractable hematological malignancy in humans. Biomedicine &amp; pharmacotherapy = Biomedecine &amp; pharmacotherapie. 2022; 149: 112864. DOI: 10.1016/j.biopha.2022.112864</mixed-citation></ref><ref id="B33"><label>33.</label><mixed-citation>Mohite P., Lokwani D.K., Sakle N.S. Exploring the therapeutic potential of SGLT2 inhibitors in cancer treatment: integrating in silico and in vitro investigations. Naunyn Schmiedebergs Arch Pharmacol. 2024; 397 (8): 6107–6119. DOI: 10.1007/s00210-024-03021-x</mixed-citation></ref><ref id="B34"><label>34.</label><mixed-citation>Luo J., Hendryx M., Dong Y. Sodium-glucose cotransporter 2 (SGLT2) inhibitors and non-small cell lung cancer survival. Br J Cancer. 2023; 128 (8): 1541–1547. DOI: 10.1038/s41416-023-02177-2</mixed-citation></ref><ref id="B35"><label>35.</label><mixed-citation>Hendryx M., Dong Y., Ndeke J.M., Luo J. Sodium-glucose cotransporter 2 (SGLT2) inhibitor initiation and hepatocellular carcinoma prognosis. PLoS One 2022; 17 (9): e0274519. DOI: 10.1371/journal.pone.0274519</mixed-citation></ref><ref id="B36"><label>36.</label><mixed-citation>Kuo H.H., Wang K.T., Chen H.H., Lai Z.Y., Lin P.L., Chuang Y.J., Liu L.Y. Cardiovascular outcomes associated with SGLT2 inhibitor therapy in patients with type 2 diabetes mellitus and cancer: a systematic review and meta-analysis. Diabetol Metab Syndr. 2024; 16 (1): 108. DOI: 10.1186/s13098-024-01354-4</mixed-citation></ref><ref id="B37"><label>37.</label><mixed-citation>Zhang Z., Dalan R., Hu Z., Wang J.W., Chew N.W., Poh K.K., Tan R.S., Soong T.W., Dai Y., Ye L., Chen X. Reactive Oxygen Species Scavenging Nanomedicine for the Treatment of Ischemic Heart Disease. Adv Mater. 2022; 34 (35): e2202169. DOI: 10.1002/adma.202202169</mixed-citation></ref><ref id="B38"><label>38.</label><mixed-citation>D'Onofrio N., Sardu C., Trotta M.C., Scisciola L., Turriziani F., Ferraraccio F., Panarese I., Petrella L., Fanelli M., Modugno P., Massetti M., Marfella L.V., Sasso F.C., Rizzo M.R., Barbieri M., Furbatto F., Minicucci F., Mauro C., Federici M., Balestrieri M.L., Paolisso G., Marfella R. Sodium-glucose co-transporter2 expression and inflammatory activity in diabetic atherosclerotic plaques: Effects of sodium-glucose co-transporter2 inhibitor treatment. Mol Metab. 2021; 54: 101337. DOI: 10.1016/j.molmet.2021.101337</mixed-citation></ref><ref id="B39"><label>39.</label><mixed-citation>Sánchez-García A., Simental-Mendía M., Millán-Alanís J.M., Simental-Mendía L.E. Effect of sodium-glucose co-transporter 2 inhibitors on lipid profile: A systematic review and meta-analysis of 48 randomized controlled trials. Pharmacol Res. 2020; 160: 105068. DOI: 10.1016/j.phrs.2020.105068</mixed-citation></ref><ref id="B40"><label>40.</label><mixed-citation>Sawada T., Uzu K., Hashimoto N., Onishi T., Takaya T., Shimane A., Taniguchi Y., Yasaka Y., Ohara T., Kawai H. Empagliflozin's Ameliorating Effect on Plasma Triglycerides: Association with Endothelial Function Recovery in Diabetic Patients with Coronary Artery Disease. J Atheroscler Thromb. 2020; 27 (7): 644–656. DOI: 10.5551/jat.50807</mixed-citation></ref><ref id="B41"><label>41.</label><mixed-citation>Lee H.F., Chan Y.H., Chuang C., Li P.R., Yeh Y.H., Hsiao F.C., Peng J.R., See L.C. Cardiovascular, renal, and lower limb outcomes in patients with type 2 diabetes after percutaneous coronary intervention and treated with sodium-glucose cotransporter 2 inhibitors vs. dipeptidyl peptidase-4 inhibitors. Eur Heart J Cardiovasc Pharmacother. 2023; 9 (4): 301–310. DOI: 10.1093/ehjcvp/pvad004</mixed-citation></ref><ref id="B42"><label>42.</label><mixed-citation>Zhang Q., Deng Z., Li T., Chen K., Zeng Z. SGLT2 inhibitor improves the prognosis of patients with coronary heart disease and prevents in-stent restenosis. Front Cardiovasc Med. 2024; 10: 1280547. DOI: 10.3389/fcvm.2023.1280547</mixed-citation></ref><ref id="B43"><label>43.</label><mixed-citation>Hashikata T., Ikutomi M., Jimba T., Shindo A., Kakuda N., Katsushika S., Yokoyama M., Kishi M., Sato T., Matsushita M., Ohnishi S., Yamasaki M. Empagliflozin attenuates neointimal hyperplasia after drug-eluting-stent implantation in patients with type 2 diabetes. Heart Vessels. 2020; 35 (10): 1378–1389. DOI: 10.1007/s00380-020-01621-0</mixed-citation></ref><ref id="B44"><label>44.</label><mixed-citation>Heyward J., Mansour O., Olson L., Singh S., Alexander G.C. Association between sodium-glucose cotransporter 2 (SGLT2) inhibitors and lower extremity amputation: A systematic review and meta-analysis. PLoS One 2020; 15 (6): e0234065. DOI: 10.1371/journal.pone.0234065</mixed-citation></ref><ref id="B45"><label>45.</label><mixed-citation>Peyton K.J., Behnammanesh G., Durante G.L., Durante W. Canagliflozin Inhibits Human Endothelial Cell Inflammation through the Induction of Heme Oxygenase-1. Int J Mol Sci. 2022; 23 (15): 8777. DOI: 10.3390/ijms23158777</mixed-citation></ref><ref id="B46"><label>46.</label><mixed-citation>Behnammanesh G., Durante G.L., Khanna Y.P., Peyton K.J., Durante W. Canagliflozin inhibits vascular smooth muscle cell proliferation and migration: Role of heme oxygenase-1. Redox Biol. 2020; 32: 101527. DOI: 10.1016/j.redox.2020.101527</mixed-citation></ref><ref id="B47"><label>47.</label><mixed-citation>Sardu C., Massetti M., Testa N., Martino L.D., Castellano G., Turriziani F., Sasso F.C., Torella M., De Feo M., Santulli G., Paolisso G., Marfella R. Effects of Sodium-Glucose Transporter 2 Inhibitors (SGLT2-I) in Patients With Ischemic Heart Disease (IHD) Treated by Coronary Artery Bypass Grafting via MiECC: Inflammatory Burden, and Clinical Outcomes at 5 Years of Follow-Up. Front Pharmacol. 2021; 12: 777083. DOI: 10.3389/fphar.2021.777083.</mixed-citation></ref><ref id="B48"><label>48.</label><mixed-citation>Paolisso P., Bergamaschi L., Santulli G., Gallinoro E., Cesaro A., Gragnano F., Sardu C., Mileva N., Foà A., Armillotta M., Sansonetti A., Amicone S., Impellizzeri A., Casella G., Mauro C., Vassilev D., Marfella R., Calabrò P., Barbato E., Pizzi C. Infarct size, inflammatory burden, and admission hyperglycemia in diabetic patients with acute myocardial infarction treated with SGLT2-inhibitors: a multicenter international registry. Cardiovasc Diabetol. 2022; 21 (1): 77. DOI: 10.1186/s12933-022-01506-8</mixed-citation></ref><ref id="B49"><label>49.</label><mixed-citation>Leask M.P., Merriman T.R. The genetic basis of urate control and gout: Insights into molecular pathogenesis from follow-up study of genome-wide association study loci. Best Pract Res Clin Rheumatol. 2021; 35 (4): 101721. DOI: 10.1016/j.berh.2021.101721</mixed-citation></ref><ref id="B50"><label>50.</label><mixed-citation>Boocock J., Leask M., Okada Y.; Asian Genetic Epidemiology Network (AGEN) Consortium; Matsuo H., Kawamura Y., Shi Y., Li C., Mount D.B., Mandal A.K., Wang W., Cadzow M., Gosling A.L., Major T.J., Horsfield J.A., Choi H.K., Fadason T., O'Sullivan J., Stahl E.A., Merriman T.R. Genomic dissection of 43 serum urate-associated loci provides multiple insights into molecular mechanisms of urate control. Hum Mol Genet. 2020; 29 (6): 923–943. DOI: 10.1093/hmg/ddaa013</mixed-citation></ref><ref id="B51"><label>51.</label><mixed-citation>Packer M. Hyperuricemia and Gout Reduction by SGLT2 Inhibitors in Diabetes and Heart Failure: JACC Review Topic of the Week. J Am Coll Cardiol. 2024; 83 (2): 371–381. DOI: 10.1016/j.jacc.2023.10.030</mixed-citation></ref><ref id="B52"><label>52.</label><mixed-citation>Packer M. SGLT2 Inhibitors Produce Cardiorenal Benefits by Promoting Adaptive Cellular Reprogramming to Induce a State of Fasting Mimicry: A Paradigm Shift in Understanding Their Mechanism of Action. Diabetes Care. 2020; 43 (3): 508–511. DOI: 10.2337/dci19-0074</mixed-citation></ref><ref id="B53"><label>53.</label><mixed-citation>Packer M. Foetal recapitulation of nutrient surplus signalling by O-GlcNAcylation and the failing heart. Eur J Heart Fail. 2023; 25 (8): 1199–1212. DOI: 10.1002/ejhf.2972</mixed-citation></ref><ref id="B54"><label>54.</label><mixed-citation>Packer M. Fetal Reprogramming of Nutrient Surplus Signaling, O-GlcNAcylation, and the Evolution of CKD. J Am Soc Nephrol. 2023; 34 (9): 1480–1491. DOI: 10.1681/ ASN.0000000000000177</mixed-citation></ref><ref id="B55"><label>55.</label><mixed-citation>Yokose C., McCormick N., Abhishek A., Dalbeth N., Pascart T., Lioté F., Gaffo A., FitzGerald J., Terkeltaub R., Sise M.E., Januzzi J.L., Wexler D.J., Choi H.K. The clinical benefits of sodium-glucose cotransporter type 2 inhibitors in people with gout. Nat Rev Rheumatol. 2024; 20 (4): 216–231. DOI: 10.1038/s41584-024-01092-x</mixed-citation></ref><ref id="B56"><label>56.</label><mixed-citation>Chung M.C., Hung P.H., Hsiao P.J., Wu L.Y., Chang C.H., Wu M.J., Shieh J.J., Chung C.J. Association of Sodium-Glucose Transport Protein 2 Inhibitor Use for Type 2 Diabetes and Incidence of Gout in Taiwan. JAMA Netw Open. 2021; 4 (11): e2135353. DOI: 10.1001/jamanetworkopen.2021.35353</mixed-citation></ref><ref id="B57"><label>57.</label><mixed-citation>McCormick N., Yokose C., Wei J., Lu N., Wexler D.J., Aviña-Zubieta J.A., De Vera M.A., Zhang Y., Choi H.K. Comparative Effectiveness of Sodium-Glucose Cotransporter-2 Inhibitors for Recurrent Gout Flares and Gout-Primary Emergency Department Visits and Hospitalizations: A General Population Cohort Study. Ann Intern Med. 2023; 176 (8): 1067–1080. DOI: 10.7326/M23-0724</mixed-citation></ref><ref id="B58"><label>58.</label><mixed-citation>Wei J., Choi H.K., Dalbeth N., Li X., Li C., Zeng C., Lei G., Zhang Y. Gout Flares and Mortality After Sodium-Glucose Cotransporter-2 Inhibitor Treatment for Gout and Type 2 Diabetes. JAMA Netw Open. 2023; 6 (8): e2330885. DOI: 10.1001/jamanetworkopen.2023.30885</mixed-citation></ref><ref id="B59"><label>59.</label><mixed-citation>Wood D.T., Waterbury N.V., Lund B.C. Sodium glucose cotransporter 2 inhibitors and gout risk: a sequence symmetry analysis. Clin Rheumatol. 2023; 42 (9): 2469–2475. DOI: 10.1007/s10067-023-06647-z</mixed-citation></ref><ref id="B60"><label>60.</label><mixed-citation>Dotinga R. SGLT2 Inhibitors Begin to Show Therapeutic Potential in Rheumatology. Medscape. Rheumatology 2024; 5.</mixed-citation></ref><ref id="B61"><label>61.</label><mixed-citation>Wagner B.R., Rao P.S. Sodium-glucose cotransporter 2 inhibitors: are they ready for prime time in the management of lupus nephritis? Curr Opin Rheumatol. 2024; 36 (3): 163–168. DOI: 10.1097/BOR.0000000000001002</mixed-citation></ref><ref id="B62"><label>62.</label><mixed-citation>Zhao X.Y., Li S.S., He Y.X., Yan L.J., Lv F., Liang Q.M., Gan Y.H., Han L.P., Xu H.D., Li Y.C., Qi Y.Y. SGLT2 inhibitors alleviated podocyte damage in lupus nephritis by decreasing inflammation and enhancing autophagy. Ann Rheum Dis. 2023; 82 (10): 1328–1340. DOI: 10.1136/ard-2023-224242</mixed-citation></ref><ref id="B63"><label>63.</label><mixed-citation>Jenkins B.J., Blagih J., Ponce-Garcia F.M., Canavan M., Gudgeon N., Eastham S., Hill D., Hanlon M.M., Ma E.H., Bishop E.L., Rees A., Cronin J.G., Jury E.C., Dimeloe S.K., Veale D.J., Thornton C.A., Vousden K.H., Finlay D.K., Fearon U., Jones G.W., Sinclair L.V., Vincent E.E., Jones N. Canagliflozin impairs T cell effector function via metabolic suppression in autoimmunity. Cell Metab. 2023; 35 (7): 1132–1146.e9. DOI: 10.1016/j.cmet.2023.05.001</mixed-citation></ref><ref id="B64"><label>64.</label><mixed-citation>Xiong Z., Liu T., Tse G., Gong M., Gladding P.A., Smaill B.H., Stiles M.K., Gillis A.M., Zhao J. A Machine Learning Aided Systematic Review and Meta-Analysis of the Relative Risk of Atrial Fibrillation in Patients With Diabetes Mellitus. Front Physiol. 2018; 9: 835. DOI: 10.3389/fphys.2018.00835</mixed-citation></ref><ref id="B65"><label>65.</label><mixed-citation>Aune D., Schlesinger S., Norat T., Riboli E. Diabetes mellitus and the risk of sudden cardiac death: A systematic review and meta-analysis of prospective studies. Nutr Metab Cardiovasc Dis. 2018; 28 (6): 543–556. DOI: 10.1016/j.numecd.2018.02.011</mixed-citation></ref><ref id="B66"><label>66.</label><mixed-citation>Liao J., Ebrahimi R., Ling Z., Meyer C., Martinek M., Sommer P., Futyma P., Di Vece D., Schratter A., Acou W.J., Zhu L., Kiuchi M.G., Liu S., Yin Y., Pürerfellner H., Templin C., Chen S. Effect of SGLT-2 inhibitors on arrhythmia events: insight from an updated secondary analysis of  &gt;  80,000 patients (the SGLT2i-Arrhythmias and Sudden Cardiac Death). Cardiovasc Diabetol. 2024; 23 (1): 78. DOI: 10.1186/s12933-024-02137-x</mixed-citation></ref><ref id="B67"><label>67.</label><mixed-citation>Zelniker T.A., Bonaca M.P., Furtado R.H.M., Mosenzon O., Kuder J.F., Murphy S.A., Bhatt D.L., Leiter L.A., McGuire D.K., Wilding J.P.H., Budaj A., Kiss R.G., Padilla F., Gause-Nilsson I., Langkilde A.M., Raz I., Sabatine M.S., Wiviott S.D. Effect of Dapagliflozin on Atrial Fibrillation in Patients With Type 2 Diabetes Mellitus: Insights From the DECLARE-TIMI 58 Trial. Circulation. 2020; 141 (15): 1227–1234. DOI: 10.1161/ CIRCULATIONAHA.119.044183</mixed-citation></ref><ref id="B68"><label>68.</label><mixed-citation>Curtain J.P., Docherty K.F., Jhund P.S., Petrie M.C., Inzucchi S.E., Køber L., Kosiborod M.N., Martinez F.A., Ponikowski P., Sabatine M.S., Bengtsson O., Langkilde A.M., Sjöstrand M., Solomon S.D., McMurray J.J.V. Effect of dapagliflozin on ventricular arrhythmias, resuscitated cardiac arrest, or sudden death in DAPA-HF. Eur Heart J. 2021; 42 (36): 3727–3738. DOI: 10.1093/eurheartj/ehab560</mixed-citation></ref><ref id="B69"><label>69.</label><mixed-citation>Gawałko M., Saljic A., Li N., Abu-Taha I., Jespersen T., Linz D., Nattel S., Heijman J., Fender A., Dobrev D. Adiposity-associated atrial fibrillation: molecular determinants, mechanisms, and clinical significance. Cardiovasc Res. 2023; 119 (3): 614–630. DOI: 10.1093/cvr/cvac093</mixed-citation></ref><ref id="B70"><label>70.</label><mixed-citation>Habibi J., Aroor A.R., Sowers J.R., Jia G., Hayden M.R., Garro M., Barron B., Mayoux E., Rector R.S., Whaley-Connell A., DeMarco V.G. Sodium glucose transporter 2 (SGLT2) inhibition with empagliflozin improves cardiac diastolic function in a female rodent model of diabetes. Cardiovasc Diabetol. 2017; 16 (1): 9. DOI: 10.1186/s12933-016-0489-z</mixed-citation></ref><ref id="B71"><label>71.</label><mixed-citation>Shao Q., Meng L., Lee S., Tse G., Gong M., Zhang Z., Zhao J., Zhao Y., Li G., Liu T. Empagliflozin, a sodium glucose co-transporter-2 inhibitor, alleviates atrial remodeling and improves mitochondrial function in high-fat</mixed-citation></ref><ref id="B72"><label>72.</label><mixed-citation>diet/streptozotocin-induced diabetic rats. Cardiovasc Diabetol. 2019; 18 (1): 165. DOI: 10.1186/s12933-019-0964-4</mixed-citation></ref></ref-list></back></article>
