SGLT2抑制剂在急性心肌梗死中的保护作用

陈诚, 张钲, 彭瑜, 等. SGLT2抑制剂在急性心肌梗死中的保护作用[J]. 临床心血管病杂志, 2024, 40(5): 411-415. doi: 10.13201/j.issn.1001-1439.2024.05.012
引用本文: 陈诚, 张钲, 彭瑜, 等. SGLT2抑制剂在急性心肌梗死中的保护作用[J]. 临床心血管病杂志, 2024, 40(5): 411-415. doi: 10.13201/j.issn.1001-1439.2024.05.012
CHEN Cheng, ZHANG Zheng, PENG Yu, et al. Protective effect of SGLT2 inhibitors in acute myocardial infarction[J]. J Clin Cardiol, 2024, 40(5): 411-415. doi: 10.13201/j.issn.1001-1439.2024.05.012
Citation: CHEN Cheng, ZHANG Zheng, PENG Yu, et al. Protective effect of SGLT2 inhibitors in acute myocardial infarction[J]. J Clin Cardiol, 2024, 40(5): 411-415. doi: 10.13201/j.issn.1001-1439.2024.05.012

SGLT2抑制剂在急性心肌梗死中的保护作用

  • 基金项目:
    国家自然科学基金项目(No:82000277、82060807)
详细信息

Protective effect of SGLT2 inhibitors in acute myocardial infarction

More Information
  • 钠-葡萄糖协同转运蛋白2(SGLT2)抑制剂是一种新型的口服降糖药,越来越多的临床研究显示SGLT2抑制剂可以改善糖尿病或非糖尿病患者的心血管预后,显示出SGLT2抑制剂的多效性。但SGLT2抑制剂在急性心肌梗死中的作用尚不明确,本文就SGLT2抑制剂在急性心肌梗死动物实验和临床研究作一综述。
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  • [1]

    Ferrannini E. Sodium-Glucose Co-transporters and Their Inhibition: Clinical Physiology[J]. Cell Metab, 2017, 26(1): 27-38. doi: 10.1016/j.cmet.2017.04.011

    [2]

    廖梦阳, 廖玉华, 余淼, 等. SGLT2抑制剂治疗心力衰竭潜在机制的新认识[J]. 临床心血管病杂志, 2022, 38(1): 1-6. https://lcxxg.whuhzzs.com/article/doi/10.13201/j.issn.1001-1439.2022.01.001

    [3]

    Bolinder J, Ljunggren Ö, Kullberg J, et al. Effects of dapagliflozin on body weight, total fat mass, and regional adipose tissue distribution in patients with type 2 diabetes mellitus with inadequate glycemic control on metformin[J]. J Clin Endocrinol Metab, 2012, 97(3): 1020-1031. doi: 10.1210/jc.2011-2260

    [4]

    Giugliano D, Longo M, Scappaticcio L, et al. SGLT-2 inhibitors and cardiorenal outcomes in patients with or without type 2 diabetes: a meta-analysis of 11 CVOTs[J]. Cardiovasc Diabetol, 2021, 20(1): 236. doi: 10.1186/s12933-021-01430-3

    [5]

    Lundin M, Ferrannini G, Mellbin L, et al. SOdium-glucose CO-transporter inhibition in patients with newly detected Glucose Abnormalities and a recent Myocardial Infarction(SOCOGAMI)[J]. Diabetes Res Clin Pract, 2022, 193: 110141. doi: 10.1016/j.diabres.2022.110141

    [6]

    Zinman B, Wanner C, Lachin J M, et al. Empagliflozin, Cardiovascular Outcomes, and Mortality in Type 2 Diabetes[J]. N Engl J Med, 2015, 373(22): 2117-2128. doi: 10.1056/NEJMoa1504720

    [7]

    Neal B, Perkovic V, Mahaffey KW, et al. Canagliflozin and Cardiovascular and Renal Events in Type 2 Diabetes[J]. N Engl J Med, 2017, 377(7): 644-657. doi: 10.1056/NEJMoa1611925

    [8]

    Bell RM, Yellon DM. SGLT2 inhibitors: hypotheses on the mechanism of cardiovascular protection[J]. Lancet Diabetes Endocrinol, 2018, 6(6): 435-437. doi: 10.1016/S2213-8587(17)30314-5

    [9]

    You L, Wang Q, Ma Y, et al. Precise dapagliflozin delivery by cardiac homing peptide functionalized mesoporous silica nanocarries for heart failure repair after myocardial infarction[J]. Front Chem, 2022, 10: 1013910. doi: 10.3389/fchem.2022.1013910

    [10]

    Zhang T, Deng W, Deng Y, et al. Mechanisms of ferroptosis regulating oxidative stress and energy metabolism in myocardial ischemia-reperfusion injury and a novel perspective of natural plant active ingredients for its treatment[J]. Biomed Pharmacother, 2023, 165: 114706. doi: 10.1016/j.biopha.2023.114706

    [11]

    Shi Y, Zhang H, Huang S, et al. Epigenetic regulation in cardiovascular disease: mechanisms and advances in clinical trials[J]. Signal Transduct Target Ther, 2022, 7(1): 200. doi: 10.1038/s41392-022-01055-2

    [12]

    Wang K, Li Z, Sun Y, et al. Dapagliflozin Improves Cardiac Function, Remodeling, Myocardial Apoptosis, and Inflammatory Cytokines in Mice with Myocardial Infarction[J]. J Cardiovasc Transl Res, 2022, 15(4): 786-796. doi: 10.1007/s12265-021-10192-y

    [13]

    Kataoka T. Biological properties of the BCL-2 family protein BCL-RAMBO, which regulates apoptosis, mitochondrial fragmentation, and mitophagy[J]. Front Cell Dev Biol, 2022, 10: 1065702. doi: 10.3389/fcell.2022.1065702

    [14]

    Goerg J, Sommerfeld M, Greiner B, et al. Low-Dose Empagliflozin Improves Systolic Heart Function after Myocardial Infarction in Rats: Regulation of MMP9, NHE1, and SERCA2a[J]. Int J Mol Sci, 2021, 22(11): 5437. doi: 10.3390/ijms22115437

    [15]

    Samuel TJ, Rosenberry RP, Lee S, et al. Correcting Calcium Dysregulation in Chronic Heart Failure Using SERCA2a Gene Therapy[J]. Int J Mol Sci, 2018, 19(4): 1086. doi: 10.3390/ijms19041086

    [16]

    Jiang K, Xu Y, Wang D, et al. Cardioprotective mechanism of SGLT2 inhibitor against myocardial infarction is through reduction of autosis[J]. Protein Cell, 2022, 13(5): 336-359. doi: 10.1007/s13238-020-00809-4

    [17]

    Xia H, Zahra A, Jia M, et al. Na(+)/H(+)Exchanger 1, a Potential Therapeutic Drug Target for Cardiac Hypertrophy and Heart Failure[J]. Pharmaceuticals(Basel), 2022, 15(7): 875. doi: 10.3390/ph15070875

    [18]

    Gong L, Wang X, Pan J, et al. The co-treatment of rosuvastatin with dapagliflozin synergistically inhibited apoptosis via activating the PI3K/AKt/mTOR signaling pathway in myocardial ischemia/reperfusion injury rats[J]. Open Med(Wars), 2021, 15(1): 47-57.

    [19]

    Yang C, Liu X, Yang F, et al. Mitochondrial phosphatase PGAM5 regulates Keap1-mediated Bcl-xL degradation and controls cardiomyocyte apoptosis driven by myocardial ischemia/reperfusion injury[J]. In Vitro Cell Dev Biol Anim, 2017, 53(3): 248-257. doi: 10.1007/s11626-016-0105-2

    [20]

    Fan ZG, Xu Y, Chen X, et al. Appropriate Dose of Dapagliflozin Improves Cardiac Outcomes by Normalizing Mitochondrial Fission and Reducing Cardiomyocyte Apoptosis After Acute Myocardial Infarction[J]. Drug Des Devel Ther, 2022, 16: 2017-2030. doi: 10.2147/DDDT.S371506

    [21]

    Ju F, Abbott GW, Li J, et al. Canagliflozin Pretreatment Attenuates Myocardial Dysfunction and Improves Postcardiac Arrest Outcomes After Cardiac Arrest and Cardiopulmonary Resuscitation in Mice[J]. Cardiovasc Drugs Ther, 2024, 38(2): 279-295. doi: 10.1007/s10557-022-07419-8

    [22]

    Guo H, Callaway JB, Ting JP. Inflammasomes: mechanism of action, role in disease, and therapeutics[J]. Nat Med, 2015, 21(7): 677-687. doi: 10.1038/nm.3893

    [23]

    Liu Y, Lian K, Zhang L, et al. TXNIP mediates NLRP3 inflammasome activation in cardiac microvascular endothelial cells as a novel mechanism in myocardial ischemia/reperfusion injury[J]. Basic Res Cardiol, 2014, 109(5): 415. doi: 10.1007/s00395-014-0415-z

    [24]

    Yu YW, Que JQ, Liu S, et al. Sodium-Glucose Co-transporter-2 Inhibitor of Dapagliflozin Attenuates Myocardial Ischemia/Reperfusion Injury by Limiting NLRP3 Inflammasome Activation and Modulating Autophagy[J]. Front Cardiovasc Med, 2021, 8: 768214.

    [25]

    Paolisso P, Bergamaschi L, Santulli G, et al. Infarct size, inflammatory burden, and admission hyperglycemia in diabetic patients with acute myocardial infarction treated with SGLT2-inhibitors: a multicenter international registry[J]. Cardiovasc Diabetol, 2022, 21(1): 77. doi: 10.1186/s12933-022-01506-8

    [26]

    Furtado R, Bonaca MP, Raz I, et al. Dapagliflozin and Cardiovascular Outcomes in Patients With Type 2 Diabetes Mellitus and Previous Myocardial Infarction[J]. Circulation, 2019, 139(22): 2516-2527. doi: 10.1161/CIRCULATIONAHA.119.039996

    [27]

    von Lewinski D, Kolesnik E, Tripolt N J, et al. Empagliflozin in acute myocardial infarction: the EMMY trial[J]. Eur Heart J, 2022, 43(41): 4421-4432. doi: 10.1093/eurheartj/ehac494

    [28]

    Dayem KA, Younis O, Zarif B, et al. Impact of dapagliflozin on cardiac function following anterior myocardial infarction in non-diabetic patients-DACAMI(a randomized controlled clinical trial)[J]. Int J Cardiol, 2023, 379: 9-14. doi: 10.1016/j.ijcard.2023.03.002

    [29]

    Di Diego JM, Antzelevitch C. Ischemic ventricular arrhythmias: experimental models and their clinical relevance[J]. Heart Rhythm, 2011, 8(12): 1963-1968. doi: 10.1016/j.hrthm.2011.06.036

    [30]

    Sattler SM, Skibsbye L, Linz D, et al. Ventricular Arrhythmias in First Acute Myocardial Infarction: Epidemiology, Mechanisms, and Interventions in Large Animal Models[J]. Front Cardiovasc Med, 2019, 6: 158. doi: 10.3389/fcvm.2019.00158

    [31]

    Liang C, Li Q, Wang K, et al. Mechanisms of ventricular arrhythmias elicited by coexistence of multiple electrophysiological remodeling in ischemia: A simulation study[J]. PLoS Comput Biol, 2022, 18(4): e1009388. doi: 10.1371/journal.pcbi.1009388

    [32]

    Deo R, Albert CM. Epidemiology and genetics of sudden cardiac death[J]. Circulation, 2012, 125(4): 620-637. doi: 10.1161/CIRCULATIONAHA.111.023838

    [33]

    Behnes M, Mashayekhi K, Weiß C, et al. Prognostic Impact of Acute Myocardial Infarction in Patients Presenting With Ventricular Tachyarrhythmias and Aborted Cardiac Arrest[J]. J Am Heart Assoc, 2018, 7(19): e010004. doi: 10.1161/JAHA.118.010004

    [34]

    Frontera A, Melillo F, Baldetti L, et al. High-Density Characterization of the Ventricular Electrical Substrate During Sinus Rhythm in Post-Myocardial Infarction Patients[J]. JACC Clin Electrophysiol, 2020, 6(7): 799-811. doi: 10.1016/j.jacep.2020.04.008

    [35]

    Tao B, Liu Z, Wei F, et al. Over-expression of Kv4.3 gene reverses cardiac remodeling and transient-outward K(+)current(Ito)reduction via CaMKⅡ inhibition in myocardial infarction[J]. Biomed Pharmacother, 2020, 132: 110896. doi: 10.1016/j.biopha.2020.110896

    [36]

    Xue G, Yang X, Zhan G, et al. Sodium-Glucose cotransporter 2 inhibitor empagliflozin decreases ventricular arrhythmia susceptibility by alleviating electrophysiological remodeling post-myocardial-infarction in mice[J]. Front Pharmacol, 2022, 13: 988408. doi: 10.3389/fphar.2022.988408

    [37]

    Hu Z, Ju F, Du L, et al. Empagliflozin protects the heart against ischemia/reperfusion-induced sudden cardiac death[J]. Cardiovasc Diabetol, 2021, 20(1): 199. doi: 10.1186/s12933-021-01392-6

    [38]

    Ferrannini E, Baldi S, Frascerra S, et al. Shift to Fatty Substrate Utilization in Response to Sodium-Glucose Cotransporter 2 Inhibition in Subjects Without Diabetes and Patients With Type 2 Diabetes[J]. Diabetes, 2016, 65(5): 1190-1195. doi: 10.2337/db15-1356

    [39]

    Cotter DG, Schugar RC, Crawford PA. Ketone body metabolism and cardiovascular disease[J]. Am J Physiol Heart Circ Physiol, 2013, 304(8): H1060-H1076. doi: 10.1152/ajpheart.00646.2012

    [40]

    Cesaro A, Gragnano F, Paolisso P, et al. In-hospital arrhythmic burden reduction in diabetic patients with acute myocardial infarction treated with SGLT2-inhibitors: Insights from the SGLT2-I AMI PROTECT study[J]. Front Cardiovasc Med, 2022, 9: 1012220. doi: 10.3389/fcvm.2022.1012220

    [41]

    lnci Ü, Güzel T. The effect of empagliflozin on index of cardio-electrophysiological balance in patients with diabetes mellitus[J]. Pacing Clin Electrophysiol, 2023, 46(1): 44-49. doi: 10.1111/pace.14621

    [42]

    Panikkath R, Reinier K, Uy-Evanado A, et al. Prolonged Tpeak-to-tend interval on the resting ECG is associated with increased risk of sudden cardiac death[J]. Circ Arrhythm Electrophysiol, 2011, 4(4): 441-447. doi: 10.1161/CIRCEP.110.960658

    [43]

    Shimizu W, Kubota Y, Hoshika Y, et al. Effects of empagliflozin versus placebo on cardiac sympathetic activity in acute myocardial infarction patients with type 2 diabetes mellitus: the EMBODY trial[J]. Cardiovasc Diabetol, 2020, 19(1): 148. doi: 10.1186/s12933-020-01127-z

    [44]

    Shanmugasundaram M, Paul T, Hashemzadeh M, et al. Outcomes of Percutaneous Coronary Intervention in Atrial Fibrillation Patients Presenting With Acute Myocardial Infarction: Analysis of Nationwide Inpatient Sample Database[J]. Cardiovasc Revasc Med, 2020, 21(7): 851-854. doi: 10.1016/j.carrev.2019.12.011

    [45]

    Engström A, Wintzell V, Melbye M, et al. Sodium-Glucose Cotransporter 2 Inhibitor Treatment and Risk of Atrial Fibrillation: Scandinavian Cohort Study[J]. Diabetes Care, 2023, 46(2): 351-360. doi: 10.2337/dc22-0714

    [46]

    Fatima K, Suri A, Rija A, et al. The Effect of Sodium-Glucose Co-Transporter 2 Inhibitors on Stroke and Atrial Fibrillation: A Systematic Review and Meta-Analysis[J]. Curr Probl Cardiol, 2023, 48(4): 101582. doi: 10.1016/j.cpcardiol.2022.101582

    [47]

    Oshima H, Miki T, Kuno A, et al. Empagliflozin, an SGLT2 Inhibitor, Reduced the Mortality Rate after Acute Myocardial Infarction with Modification of Cardiac Metabolomes and Antioxidants in Diabetic Rats[J]. J Pharmacol Exp Ther, 2019, 368(3): 524-534. doi: 10.1124/jpet.118.253666

    [48]

    Aubert G, Martin OJ, Horton JL, et al. The Failing Heart Relies on Ketone Bodies as a Fuel[J]. Circulation, 2016, 133(8): 698-705. doi: 10.1161/CIRCULATIONAHA.115.017355

    [49]

    Yurista SR, Silljé H, Oberdorf-Maass SU, et al. Sodium-glucose co-transporter 2 inhibition with empagliflozin improves cardiac function in non-diabetic rats with left ventricular dysfunction after myocardial infarction[J]. Eur J Heart Fail, 2019, 21(7): 862-873. doi: 10.1002/ejhf.1473

    [50]

    Verma S, Rawat S, Ho KL, et al. Empagliflozin Increases Cardiac Energy Production in Diabetes: Novel Translational Insights Into the Heart Failure Benefits of SGLT2 Inhibitors[J]. JACC Basic Transl Sci, 2018, 3(5): 575-587. doi: 10.1016/j.jacbts.2018.07.006

    [51]

    Santos-Gallego CG, Requena-Ibanez JA, San Antonio R, et al. Empagliflozin Ameliorates Adverse Left Ventricular Remodeling in Nondiabetic Heart Failure by Enhancing Myocardial Energetics[J]. J Am Coll Cardiol, 2019, 73(15): 1931-1944. doi: 10.1016/j.jacc.2019.01.056

    [52]

    Li X, Lu Q, Qiu Y, et al. Direct Cardiac Actions of the Sodium Glucose Co-Transporter 2 Inhibitor Empagliflozin Improve Myocardial Oxidative Phosphorylation and Attenuate Pressure-Overload Heart Failure[J]. J Am Heart Assoc, 2021, 10(6): e018298. doi: 10.1161/JAHA.120.018298

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出版历程
收稿日期:  2023-06-08
刊出日期:  2024-05-13

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