An Overview of the Cardiorenal Protective Mechanisms of SGLT2 Inhibitors
Sodium-glucose co-transporter 2 (SGLT2) inhibitors block glucose reabsorption in the renal proximal tubule, an insulin-independent mechanism that plays a critical role in glycemic regulation in diabetes. In addition to their glucose-lowering effects, SGLT2 inhibitors prevent both renal damage and th...
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| Published in | International journal of molecular sciences Vol. 23; no. 7; p. 3651 |
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| Main Authors | , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Switzerland
MDPI AG
26.03.2022
MDPI |
| Subjects | |
| Online Access | Get full text |
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| Abstract | Sodium-glucose co-transporter 2 (SGLT2) inhibitors block glucose reabsorption in the renal proximal tubule, an insulin-independent mechanism that plays a critical role in glycemic regulation in diabetes. In addition to their glucose-lowering effects, SGLT2 inhibitors prevent both renal damage and the onset of chronic kidney disease and cardiovascular events, in particular heart failure with both reduced and preserved ejection fraction. These unexpected benefits prompted changes in treatment guidelines and scientific interest in the underlying mechanisms. Aside from the target effects of SGLT2 inhibition, a wide spectrum of beneficial actions is described for the kidney and the heart, even though the cardiac tissue does not express SGLT2 channels. Correction of cardiorenal risk factors, metabolic adjustments ameliorating myocardial substrate utilization, and optimization of ventricular loading conditions through effects on diuresis, natriuresis, and vascular function appear to be the main underlying mechanisms for the observed cardiorenal protection. Additional clinical advantages associated with using SGLT2 inhibitors are antifibrotic effects due to correction of inflammation and oxidative stress, modulation of mitochondrial function, and autophagy. Much research is required to understand the numerous and complex pathways involved in SGLT2 inhibition. This review summarizes the current known mechanisms of SGLT2-mediated cardiorenal protection. |
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| AbstractList | Sodium-glucose co-transporter 2 (SGLT2) inhibitors block glucose reabsorption in the renal proximal tubule, an insulin-independent mechanism that plays a critical role in glycemic regulation in diabetes. In addition to their glucose-lowering effects, SGLT2 inhibitors prevent both renal damage and the onset of chronic kidney disease and cardiovascular events, in particular heart failure with both reduced and preserved ejection fraction. These unexpected benefits prompted changes in treatment guidelines and scientific interest in the underlying mechanisms. Aside from the target effects of SGLT2 inhibition, a wide spectrum of beneficial actions is described for the kidney and the heart, even though the cardiac tissue does not express SGLT2 channels. Correction of cardiorenal risk factors, metabolic adjustments ameliorating myocardial substrate utilization, and optimization of ventricular loading conditions through effects on diuresis, natriuresis, and vascular function appear to be the main underlying mechanisms for the observed cardiorenal protection. Additional clinical advantages associated with using SGLT2 inhibitors are antifibrotic effects due to correction of inflammation and oxidative stress, modulation of mitochondrial function, and autophagy. Much research is required to understand the numerous and complex pathways involved in SGLT2 inhibition. This review summarizes the current known mechanisms of SGLT2-mediated cardiorenal protection. Sodium-glucose co-transporter 2 (SGLT2) inhibitors block glucose reabsorption in the renal proximal tubule, an insulin-independent mechanism that plays a critical role in glycemic regulation in diabetes. In addition to their glucose-lowering effects, SGLT2 inhibitors prevent both renal damage and the onset of chronic kidney disease and cardiovascular events, in particular heart failure with both reduced and preserved ejection fraction. These unexpected benefits prompted changes in treatment guidelines and scientific interest in the underlying mechanisms. Aside from the target effects of SGLT2 inhibition, a wide spectrum of beneficial actions is described for the kidney and the heart, even though the cardiac tissue does not express SGLT2 channels. Correction of cardiorenal risk factors, metabolic adjustments ameliorating myocardial substrate utilization, and optimization of ventricular loading conditions through effects on diuresis, natriuresis, and vascular function appear to be the main underlying mechanisms for the observed cardiorenal protection. Additional clinical advantages associated with using SGLT2 inhibitors are antifibrotic effects due to correction of inflammation and oxidative stress, modulation of mitochondrial function, and autophagy. Much research is required to understand the numerous and complex pathways involved in SGLT2 inhibition. This review summarizes the current known mechanisms of SGLT2-mediated cardiorenal protection.Sodium-glucose co-transporter 2 (SGLT2) inhibitors block glucose reabsorption in the renal proximal tubule, an insulin-independent mechanism that plays a critical role in glycemic regulation in diabetes. In addition to their glucose-lowering effects, SGLT2 inhibitors prevent both renal damage and the onset of chronic kidney disease and cardiovascular events, in particular heart failure with both reduced and preserved ejection fraction. These unexpected benefits prompted changes in treatment guidelines and scientific interest in the underlying mechanisms. Aside from the target effects of SGLT2 inhibition, a wide spectrum of beneficial actions is described for the kidney and the heart, even though the cardiac tissue does not express SGLT2 channels. Correction of cardiorenal risk factors, metabolic adjustments ameliorating myocardial substrate utilization, and optimization of ventricular loading conditions through effects on diuresis, natriuresis, and vascular function appear to be the main underlying mechanisms for the observed cardiorenal protection. Additional clinical advantages associated with using SGLT2 inhibitors are antifibrotic effects due to correction of inflammation and oxidative stress, modulation of mitochondrial function, and autophagy. Much research is required to understand the numerous and complex pathways involved in SGLT2 inhibition. This review summarizes the current known mechanisms of SGLT2-mediated cardiorenal protection. |
| Author | Salvatore, Teresa Di Martino, Anna Sasso, Ferdinando Carlo Di Salvo, Jessica Epifani, Raffaella Marfella, Raffaele Lettieri, Miriam Rinaldi, Luca Galiero, Raffaele Docimo, Giovanni Caturano, Alfredo Sardu, Celestino Albanese, Gaetana |
| AuthorAffiliation | 4 Division of Cardiovascular Sciences, Faculty of Biology, Medicine and Health, The University of Manchester, 3.31 Core Technology Facility, 46 Grafton Street, Manchester M13 9NT, UK; miriam.lettieri@manchester.ac.uk 1 Department of Precision Medicine, University of Campania Luigi Vanvitelli, Via De Crecchio 7, 80138 Naples, Italy; teresa.salvatore@unicampania.it 2 Department of Advanced Medical and Surgical Sciences, University of Campania Luigi Vanvitelli, Piazza Luigi Miraglia 2, 80138 Naples, Italy; raffaele.galiero@unicampania.it (R.G.); alfredo.caturano@unicampania.it (A.C.); luca.rinaldi@unicampania.it (L.R.); annadimarti@alice.it (A.D.M.); gaetanaalbanese@hotmail.it (G.A.); jessydisalvo@hotmail.it (J.D.S.); ellaphane@gmail.com (R.E.); raffaele.marfella@unicampania.it (R.M.); giovanni.docimo@unicampania.it (G.D.); celestino.sardu@unicampania.it (C.S.) 3 Mediterrannea Cardiocentro, 80122 Napoli, Italy |
| AuthorAffiliation_xml | – name: 1 Department of Precision Medicine, University of Campania Luigi Vanvitelli, Via De Crecchio 7, 80138 Naples, Italy; teresa.salvatore@unicampania.it – name: 3 Mediterrannea Cardiocentro, 80122 Napoli, Italy – name: 2 Department of Advanced Medical and Surgical Sciences, University of Campania Luigi Vanvitelli, Piazza Luigi Miraglia 2, 80138 Naples, Italy; raffaele.galiero@unicampania.it (R.G.); alfredo.caturano@unicampania.it (A.C.); luca.rinaldi@unicampania.it (L.R.); annadimarti@alice.it (A.D.M.); gaetanaalbanese@hotmail.it (G.A.); jessydisalvo@hotmail.it (J.D.S.); ellaphane@gmail.com (R.E.); raffaele.marfella@unicampania.it (R.M.); giovanni.docimo@unicampania.it (G.D.); celestino.sardu@unicampania.it (C.S.) – name: 4 Division of Cardiovascular Sciences, Faculty of Biology, Medicine and Health, The University of Manchester, 3.31 Core Technology Facility, 46 Grafton Street, Manchester M13 9NT, UK; miriam.lettieri@manchester.ac.uk |
| Author_xml | – sequence: 1 givenname: Teresa surname: Salvatore fullname: Salvatore, Teresa – sequence: 2 givenname: Raffaele orcidid: 0000-0002-7766-3430 surname: Galiero fullname: Galiero, Raffaele – sequence: 3 givenname: Alfredo orcidid: 0000-0001-7761-7533 surname: Caturano fullname: Caturano, Alfredo – sequence: 4 givenname: Luca orcidid: 0000-0002-6541-3821 surname: Rinaldi fullname: Rinaldi, Luca – sequence: 5 givenname: Anna surname: Di Martino fullname: Di Martino, Anna – sequence: 6 givenname: Gaetana surname: Albanese fullname: Albanese, Gaetana – sequence: 7 givenname: Jessica surname: Di Salvo fullname: Di Salvo, Jessica – sequence: 8 givenname: Raffaella surname: Epifani fullname: Epifani, Raffaella – sequence: 9 givenname: Raffaele orcidid: 0000-0003-3960-9270 surname: Marfella fullname: Marfella, Raffaele – sequence: 10 givenname: Giovanni surname: Docimo fullname: Docimo, Giovanni – sequence: 11 givenname: Miriam surname: Lettieri fullname: Lettieri, Miriam – sequence: 12 givenname: Celestino surname: Sardu fullname: Sardu, Celestino – sequence: 13 givenname: Ferdinando Carlo orcidid: 0000-0002-9142-7848 surname: Sasso fullname: Sasso, Ferdinando Carlo |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/35409011$$D View this record in MEDLINE/PubMed |
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| Title | An Overview of the Cardiorenal Protective Mechanisms of SGLT2 Inhibitors |
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