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Guest Editor

Outpatient Department of Cardiometabolic Medicine, Second Department of Cardiology, Aristotle University of Thessaloniki, General Hospital “Hippokration”, 57001 Thessaloniki, Greece
Interests: type 2 diabetes mellitus; diabetic complications; cardiovascular disease; heart failure; chronic kidney disease
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Dr. Nikolaos Fragakis

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2nd Cardiology Department, Hippokration General Hospital, Aristotle University Medical School, Κonstantinoupoleos 49, 54642 Thessaloniki, PK, Greece
Interests: cardiology; electrophysiology; cardiometabolic medicine

Special Issue Information

Dear Colleagues,

Cardiometabolic Medicine is an emerging scientific field, attracting physicians across the spectrum of medical specialties, such as Internal Medicine, Cardiology, Endocrinology and Diabetology, and Nephrology. It is clear that type 2 diabetes mellitus constitutes the metabolic pandemic of the 21st century, with pessimistic projections regarding its prevalence. In addition, type 2 diabetes mellitus is associated with several comorbidities, such as hypertension, dyslipidemia, atherosclerotic cardiovascular disease, heart failure, chronic kidney disease, obesity, nonalcoholic fatty liver disease and nonalcoholic steatohepatitis, hyperuricemia, and several others. Some of them are coincident, while others are mostly complications of underlying diabetes mellitus.

During the last decade, welcome novel classes of antidiabetic drugs have arrived, which have provided remarkable cardiorenal benefits for individuals with type 2 diabetes mellitus, revolutionizing its therapeutic approach. In addition, current treatment guedelines have widely adopted those drug classes across a wide spectrum of comorbidities, even in the absence of type 2 diabetes mellitus at baseline.

This Special Issue will publish high-quality original articles addressing the evolving role of newer antidiabetics in cardiometabolic health in type 2 diabetes mellitus, from pathophysiology to treatment, emphasizing molecular pathways and their therapeutic implications. In addition, narrative reviews and systematic reviews with or without meta-analyses will be considered for publication.

Dr. Dimitrios Patoulias
Dr. Nikolaos Fragakis
Guest Editors

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Keywords

type 2 diabetes mellitus
cardiovascular disease
chronic kidney disease
SGLT-2 inhibitor
GLP-1 receptor agonist
dual GLP-1/GIP receptor agonist
pathophysiology
treatment

Published Papers (2 papers)

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Research

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Open AccessArticle

Glucagon-like Peptide-1 Receptor Activation Reduces Pulmonary Vein Arrhythmogenesis and Regulates Calcium Homeostasis

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Int. J. Mol. Sci. 2023, 24(17), 13100; https://doi.org/10.3390/ijms241713100 - 23 Aug 2023

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Abstract

Glucagon-like peptide-1 (GLP-1) receptor agonists are associated with reduced atrial fibrillation risk, but the mechanisms underlying this association remain unclear. The GLP-1 receptor agonist directly impacts cardiac Ca²⁺ homeostasis, which is crucial in pulmonary vein (PV, the initiator of atrial fibrillation) arrhythmogenesis. This study investigated the effects of the GLP-1 receptor agonist on PV electrophysiology and Ca²⁺ homeostasis and elucidated the potential underlying mechanisms. Conventional microelectrodes and whole-cell patch clamp techniques were employed in rabbit PV tissues and single PV cardiomyocytes before and after GLP-1 (7-36) amide, a GLP-1 receptor agonist. Evaluations were conducted both with and without pretreatment with H89 (10 μM, an inhibitor of protein kinase A, PKA), KN93 (1 μM, an inhibitor of Ca²⁺/calmodulin-dependent protein kinase II, CaMKII), and KB-R7943 (10 μM, an inhibitor of Na⁺/Ca²⁺ exchanger, NCX). Results showed that GLP-1 (7-36) amide (at concentrations of 1, 10, and 100 nM) reduced PV spontaneous activity in a concentration-dependent manner without affecting sinoatrial node electrical activity. In single-cell experiments, GLP-1 (7-36) amide (at 10 nM) reduced L-type Ca²⁺ current, NCX current, and late Na⁺ current in PV cardiomyocytes without altering Na⁺ current. Additionally, GLP-1 (7-36) amide (at 10 nM) increased sarcoplasmic reticulum Ca²⁺ content in PV cardiomyocytes. Furthermore, the antiarrhythmic effects of GLP-1 (7-36) amide on PV automaticity were diminished when pretreated with H89, KN93, or KB-R7943. This suggests that the GLP-1 receptor agonist may exert its antiarrhythmic potential by regulating PKA, CaMKII, and NCX activity, as well as modulating intracellular Ca²⁺ homeostasis, thereby reducing PV arrhythmogenesis. Full article

(This article belongs to the Special Issue Newer Antidiabetics and Cardio-Metabolic Health: From Pathophysiology to Treatment)

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Review

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Open AccessReview

The Impact of SGLT2 Inhibitors in the Heart and Kidneys Regardless of Diabetes Status

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Int. J. Mol. Sci. 2023, 24(18), 14243; https://doi.org/10.3390/ijms241814243 - 18 Sep 2023

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Abstract

Chronic Kidney Disease (CKD) and Cardiovascular Disease (CVD) are two devastating diseases that may occur in nondiabetics or individuals with diabetes and, when combined, it is referred to as cardiorenal disease. The impact of cardiorenal disease on society, the economy and the healthcare system is enormous. Although there are numerous therapies for cardiorenal disease, one therapy showing a great deal of promise is sodium-dependent glucose cotransporter 2 (SGLT2) inhibitors. The SGLT family member, SGLT2, is often implicated in the pathogenesis of a range of diseases, and the dysregulation of the activity of SGLT2 markedly effects the transport of glucose and sodium across the luminal membrane of renal cells. Inhibitors of SGLT2 were developed based on the antidiabetic action initiated by inhibiting renal glucose reabsorption, thereby increasing glucosuria. Of great medical significance, large-scale clinical trials utilizing a range of SGLT2 inhibitors have demonstrated both metabolic and biochemical benefits via numerous novel mechanisms, such as sympathoinhibition, which will be discussed in this review. In summary, SGLT2 inhibitors clearly exert cardio-renal protection in people with and without diabetes in both preclinical and clinical settings. This exciting class of inhibitors improve hyperglycemia, high blood pressure, hyperlipidemia and diabetic retinopathy via multiple mechanisms, of which many are yet to be elucidated. Full article

(This article belongs to the Special Issue Newer Antidiabetics and Cardio-Metabolic Health: From Pathophysiology to Treatment)

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