Benefits of SGLT2 inhibitors in arrhythmias

被引:21
作者
Gao, Jinghan [1 ]
Xue, Genlong [1 ]
Zhan, Ge [1 ]
Wang, Xinying [1 ]
Li, Jiatian [1 ]
Yang, Xiaolei [1 ]
Xia, Yunlong [1 ]
机构
[1] Dalian Med Univ, Affiliated Hosp 1, Dept Cardiol, Dalian, Liaoning, Peoples R China
基金
中国国家自然科学基金;
关键词
SGLT2; inhibitors; arrhythmia; electrical remodeling; structural remodeling; mechanisms; COTRANSPORTER; 2; INHIBITOR; TYPE-2; DIABETES-MELLITUS; ACTIVATED PROTEIN-KINASE; ATRIAL-FIBRILLATION; HEART-FAILURE; CELL-DEATH; CARDIAC FIBROSIS; NA+/CA2+ EXCHANGE; INTRACELLULAR NA+; REDOX REGULATION;
D O I
10.3389/fcvm.2022.1011429
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Some studies have shown that sodium-glucose cotransporter (SGLT) 2 inhibitors can definitively attenuate the occurrence of cardiovascular diseases such as heart failure (HF), dilated cardiomyopathy (DCM), and myocardial infarction. With the development of research, SGLT2 inhibitors can also reduce the risk of arrhythmias. So in this review, how SGLT2 inhibitors play a role in reducing the risk of arrhythmia from the perspective of electrical remodeling and structural remodeling are explored and then the possible mechanisms are discussed. Specifically, we focus on the role of SGLT2 inhibitors in Na+ and Ca2 + homeostasis and the transients of Na+ and Ca2 +, which could affect electrical remodeling and then lead to arrythmia. We also discuss the protective role of SGLT2 inhibitors in structural remodeling from the perspective of fibrosis, inflammation, oxidative stress, and apoptosis. Ultimately, it is clear that SGLT2 inhibitors have significant benefits on cardiovascular diseases such as HF, myocardial hypertrophy and myocardial infarction. It can be expected that SGLT2 inhibitors can reduce the risk of arrhythmia.
引用
收藏
页数:13
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共 163 条
[1]   Empagliflozin Limits Myocardial Infarction in Vivo and Cell Death in Vitro: Role of STAT3, Mitochondria, and Redox Aspects [J].
Andreadou, Ioanna ;
Efentakis, Panagiotis ;
Balafas, Evangelos ;
Togliatto, Gabriele ;
Davos, Constantinos H. ;
Varela, Aimilia ;
Dimitriou, Constantinos A. ;
Nikolaou, Panagiota-Efstathia ;
Maratou, Eirini ;
Lambadiari, Vaia ;
Ikonomidis, Ignatios ;
Kostomitsopoulos, Nikolaos ;
Brizzi, Maria F. ;
Dimitriadis, George ;
Iliodromitis, Efstathios K. .
FRONTIERS IN PHYSIOLOGY, 2017, 8
[2]   Empagliflozin in Heart Failure with a Preserved Ejection Fraction [J].
Anker, Stefan D. ;
Butler, Javed ;
Filippatos, Gerasimos ;
Ferreira, Joao P. ;
Bocchi, Edimar ;
Boehm, Michael ;
Brunner-La Rocca, Hans-Peter ;
Choi, Dong-Ju ;
Chopra, Vijay ;
Chuquiure-Valenzuela, Eduardo ;
Giannetti, Nadia ;
Gomez-Mesa, Juan Esteban ;
Janssens, Stefan ;
Januzzi, James L. ;
Gonzalez-Juanatey, Jose R. ;
Merkely, Bela ;
Nicholls, Stephen J. ;
Perrone, Sergio V. ;
Pina, Ileana L. ;
Ponikowski, Piotr ;
Senni, Michele ;
Sim, David ;
Spinar, Jindrich ;
Squire, Iain ;
Taddei, Stefano ;
Tsutsui, Hiroyuki ;
Verma, Subodh ;
Vinereanu, Dragos ;
Zhang, Jian ;
Carson, Peter ;
Lam, Carolyn Su Ping ;
Marx, Nikolaus ;
Zeller, Cordula ;
Sattar, Naveed ;
Jamal, Waheed ;
Schnaidt, Sven ;
Schnee, Janet M. ;
Brueckmann, Martina ;
Pocock, Stuart J. ;
Zannad, Faiez ;
Packer, Milton .
NEW ENGLAND JOURNAL OF MEDICINE, 2021, 385 (16) :1451-1461
[3]   Intracellular sodium increase and susceptibility to ischaemia in hearts from type 2 diabetic db/db mice [J].
Anzawa, R ;
Bernard, M ;
Tamareille, S ;
Baetz, D ;
Confort-Gouny, S ;
Gascard, JP ;
Cozzone, P ;
Feuvray, D .
DIABETOLOGIA, 2006, 49 (03) :598-606
[4]   Serum and glucocorticoid-responsive kinase-1 regulates cardiomyocyte survival and hypertrophic response [J].
Aoyama, T ;
Matsui, T ;
Novikov, M ;
Park, J ;
Hemmings, B ;
Rosenzweig, A .
CIRCULATION, 2005, 111 (13) :1652-1659
[5]   Empagliflozin reduces the levels of CD36 and cardiotoxic lipids while improving autophagy in the hearts of Zucker diabetic fatty rats [J].
Aragon-Herrera, Alana ;
Feijoo-Bandin, Sandra ;
Santiago, Manuel Otero ;
Barral, Luis ;
Campos-Toimil, Manuel ;
Gil-Longo, Jose ;
Pereira, Thiago M. Costa ;
Garcia-Caballero, Tomas ;
Rodriguez-Segade, Santiago ;
Rodriguez, Javier ;
Tarazon, Estefania ;
Rosello-Lleti, Esther ;
Portoles, Manuel ;
Gualillo, Oreste ;
Ramon Gonzalez-Juanatey, Jose ;
Lago, Francisca .
BIOCHEMICAL PHARMACOLOGY, 2019, 170
[6]   Sodium-glucose cotransporter 2 inhibitor Dapagliflozin attenuates diabetic cardiomyopathy [J].
Arow, M. ;
Waldman, M. ;
Yadin, D. ;
Nudelman, V. ;
Shainberg, A. ;
Abraham, N. G. ;
Freimark, D. ;
Kornowski, R. ;
Aravot, D. ;
Hochhauser, E. ;
Arad, M. .
CARDIOVASCULAR DIABETOLOGY, 2020, 19 (01)
[7]   Reinterpreting Cardiorenal Protection of Renal Sodium-Glucose Cotransporter 2 Inhibitors via Cellular Life History Programming [J].
Avogaro, Angelo ;
Fadini, Gian Paolo ;
Del Prato, Stefano .
DIABETES CARE, 2020, 43 (03) :501-507
[8]   [Na+]i and the driving force of the Na+/Ca2+-exchanger in heart failure [J].
Baartscheer, A ;
Schumacher, CA ;
Belterman, CNW ;
Coronel, R ;
Fiolet, JWT .
CARDIOVASCULAR RESEARCH, 2003, 57 (04) :986-995
[9]   Empagliflozin decreases myocardial cytoplasmic Na+ through inhibition of the cardiac Na+/H+ exchanger in rats and rabbits [J].
Baartscheer, Antonius ;
Schumacher, Cees A. ;
Wust, Rob C. I. ;
Fiolet, Jan W. T. ;
Stienen, Ger J. M. ;
Coronel, Ruben ;
Zuurbier, Coert J. .
DIABETOLOGIA, 2017, 60 (03) :568-573
[10]   Intracellular Na+ and cardiac metabolism [J].
Bay, Johannes ;
Kohlhaas, Michael ;
Maack, Christoph .
JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY, 2013, 61 :20-27