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Tytuł pozycji:

Cardioprotection by SGLT2 Inhibitors-Does It All Come Down to Na + ?

Tytuł:
Cardioprotection by SGLT2 Inhibitors-Does It All Come Down to Na ?
Autorzy:
Trum M; Department of Internal Medicine II, University Hospital Regensburg, 93053 Regensburg, Germany.
Riechel J; Department of Internal Medicine II, University Hospital Regensburg, 93053 Regensburg, Germany.
Wagner S; Department of Internal Medicine II, University Hospital Regensburg, 93053 Regensburg, Germany.
Źródło:
International journal of molecular sciences [Int J Mol Sci] 2021 Jul 26; Vol. 22 (15). Date of Electronic Publication: 2021 Jul 26.
Typ publikacji:
Journal Article; Review
Język:
English
Imprint Name(s):
Original Publication: Basel, Switzerland : MDPI, [2000-
MeSH Terms:
Arrhythmias, Cardiac/*drug therapy
Cardiotonic Agents/*therapeutic use
Myocardium/*metabolism
Myocytes, Cardiac/*metabolism
Sodium-Glucose Transporter 2/*metabolism
Sodium-Glucose Transporter 2 Inhibitors/*therapeutic use
Animals ; Arrhythmias, Cardiac/metabolism ; Arrhythmias, Cardiac/pathology ; Humans ; Myocardium/pathology ; Myocytes, Cardiac/pathology
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Contributed Indexing:
Keywords: CaMKII; HFpEF; HFrEF; NHE1; Na+; SGLT2 inhibitor; arrhythmia; heart failure; late INa
Substance Nomenclature:
0 (Cardiotonic Agents)
0 (SLC5A2 protein, human)
0 (Sodium-Glucose Transporter 2)
0 (Sodium-Glucose Transporter 2 Inhibitors)
Entry Date(s):
Date Created: 20210807 Date Completed: 20210908 Latest Revision: 20210908
Update Code:
20240105
PubMed Central ID:
PMC8347698
DOI:
10.3390/ijms22157976
PMID:
34360742
Czasopismo naukowe
Sodium-glucose co-transporter 2 inhibitors (SGLT2i) are emerging as a new treatment strategy for heart failure with reduced ejection fraction (HFrEF) and-depending on the wistfully awaited results of two clinical trials (DELIVER and EMPEROR-Preserved)-may be the first drug class to improve cardiovascular outcomes in patients suffering from heart failure with preserved ejection fraction (HFpEF). Proposed mechanisms of action of this class of drugs are diverse and include metabolic and hemodynamic effects as well as effects on inflammation, neurohumoral activation, and intracellular ion homeostasis. In this review we focus on the growing body of evidence for SGLT2i-mediated effects on cardiac intracellular Na + as an upstream mechanism. Therefore, we will first give a short overview of physiological cardiomyocyte Na + handling and its deterioration in heart failure. On this basis we discuss the salutary effects of SGLT2i on Na + homeostasis by influencing NHE1 activity, late I Na as well as CaMKII activity. Finally, we highlight the potential relevance of these effects for systolic and diastolic dysfunction as well as arrhythmogenesis.
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