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Molecular and Pathophysiological Insights into the Pleiotropic Role of SGLT2i
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Molecular and Pathophysiological Insights into the Pleiotropic Role of SGLT2i

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (31 October 2024) | Viewed by 2610

Special Issue Editor

Dr. Andrea D'Amato

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Guest Editor
1. Department of Clinical, Internal, Anesthesiology and Cardiovascular Sciences, Sapienza University of Rome, Viale del Policlinico, Rome, Italy
2. Cardiology Unit, Fabrizio Spaziani Hospital, Frosinone, Italy
Interests: acute heart failure; chronic heart failure; biomarkers; pharmacology; coronary microvascular dysfunction
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Cardiovascular diseases are one of the main causes of morbidity and mortality worldwide, destined to increase their diffusion due to the aging of the world population. Over the last decades, there has been improvement in therapy, leaving a great impact on HF patients’ prognosis, especially in ones affected by HFrEF.

Among the latest additions to HF medical therapy are SGLT2 inhibitors (SGLT2i). Initially, these drugs were developed as anti-hyperglycemic drugs for type II diabetes therapy, but they were also found to be effective in the treatment of other clinical conditions such as heart failure and chronic kidney disease. Regarding their role in heart failure, clinical trials have shown SGLT2i to reduce CV events and mortality in patients with HF, improving cardiac metabolism, reducing cardiomyocytes injury and attenuating adverse cardiac remodeling. Based on the promising outcome of clinical trials, SGLT2i has been included in the four pillars of treatment for HFrEF, also becoming the first disease-modifying drug for HFpEF.

To better highlight the recent advances, this Special Issue will focus on the molecular and pathophysiological aspects of SGLT2i, considering their pleiotropic effects.

Specifically, original articles reporting completely new results or reviews of current literature on this aspect will be taken into account. The Special Issue aims to highlight both basic and translational research to allow for a more complete comprehension of the role of SGLT2i in the field of cardiovascular diseases.

Dr. Andrea D’Amato
Guest Editor

Manuscript Submission Information

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Keywords

  • sodium–glucose transport protein 2
  • SGLT2i
  • heart failure
  • myocardial remodeling
  • myocardial infarction
  • myocarditis
  • diabetic cardiomyopathy
  • molecular signaling
  • therapeutic benefits
  • kidneys

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Published Papers (3 papers)

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Research

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13 pages, 1104 KiB  
Article
Effects of SGLT2-Inhibitors on Comprehensive Geriatric Assessment, Biomarkers of Oxidative Stress, and Platelet Activation in Elderly Diabetic Patients with Heart Failure with Preserved Ejection Fraction
by Marcello Magurno, Velia Cassano, Francesco Maruca, Carlo Alberto Pastura, Marcello Divino, Federica Fazio, Giandomenico Severini, Elvira Clausi, Giuseppe Armentaro, Sofia Miceli, Raffaele Maio, Egidio Imbalzano, Francesco Andreozzi, Marta Letizia Hribal and Angela Sciacqua
Int. J. Mol. Sci. 2024, 25(16), 8811; https://doi.org/10.3390/ijms25168811 - 13 Aug 2024
Cited by 1 | Viewed by 951
Abstract
Background: Heart failure (HF) with preserved ejection fraction (HFpEF) represents a major comorbidity in the elderly and is associated with cognitive impairment (CoI) and type 2 diabetes mellitus (T2DM). In this context, there is an increase in oxidative stress and platelet activation biomarkers. [...] Read more.
Background: Heart failure (HF) with preserved ejection fraction (HFpEF) represents a major comorbidity in the elderly and is associated with cognitive impairment (CoI) and type 2 diabetes mellitus (T2DM). In this context, there is an increase in oxidative stress and platelet activation biomarkers. The aim of this study was to evaluate the effects of 6 months’ treatment with SGLT2i on functional, mood-related, and cognitive aspects, assessed by performing a comprehensive geriatric assessment (CGA), and on oxidative stress and platelet activation biomarkers, in a cohort of HFpEF elderly patients with T2DM. We recruited 150 elderly outpatients (mean age 75.8 ± 7.4 years). Results: At six-month follow-up, there was a significant improvement in MMSE (p < 0.0001), MoCA (p < 0.0001), GDS score (p < 0.0001), and SPPB (p < 0.0001). Moreover, we observed a significant reduction in Nox-2 (p < 0.0001), 8-Isoprostane (p < 0.0001), Sp-Selectin (p < 0.0001), and Gp-VI (p < 0.0001). Considering ΔMMSE as the dependent variable, ΔE/e’, ΔNox-2, ΔHOMA, Δ8-Isoprostane, and ΔUricemia were associated for 59.6% with ΔMMSE. When ΔMoCA was considered as the dependent variable, ΔHOMA, ΔE/e’, Δ8-Isoprostane, ΔNox-2 and ΔUricemia were associated for 59.2%. Considering ΔGDS as the dependent variable, ΔHOMA, ΔNox-2, Δ8-Isoprostane, and ΔUricemia were associated with 41.6% of ΔGDS variation. Finally, ΔHOMA was the main predictor of ΔSPPB, which was associated with 21.3% with ΔSPPB, Δ8-Isoprostane, ΔNox-2, ΔE/e’, and ΔUricemia added another 24.1%. Conclusion: The use of SGLT2i in elderly patients with T2DM and HFpEF significantly contributes to improving CGA scales and biomarkers of OS and PA. Full article
(This article belongs to the Special Issue Molecular and Pathophysiological Insights into the Pleiotropic Role of SGLT2i)
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14 pages, 2457 KiB  
Article
Empagliflozin Prevent High-Glucose Stimulation Inducing Apoptosis and Mitochondria Fragmentation in H9C2 Cells through the Calcium-Dependent Activation Extracellular Signal-Regulated Kinase 1/2 Pathway
by Yung-Lung Chen, Hui-Ting Wang, Wen-Chin Lee, Pei-Ting Lin, Wen-Hao Liu and Shu-Kai Hsueh
Int. J. Mol. Sci. 2024, 25(15), 8235; https://doi.org/10.3390/ijms25158235 - 28 Jul 2024
Viewed by 784
Abstract
A previous study showed that high-glucose (HG) conditions induce mitochondria fragmentation through the calcium-mediated activation of extracellular signal-regulated kinase 1/2 (ERK 1/2) in H9C2 cells. This study tested whether empagliflozin could prevent HG-induced mitochondria fragmentation through this pathway. We found that exposing H9C2 [...] Read more.
A previous study showed that high-glucose (HG) conditions induce mitochondria fragmentation through the calcium-mediated activation of extracellular signal-regulated kinase 1/2 (ERK 1/2) in H9C2 cells. This study tested whether empagliflozin could prevent HG-induced mitochondria fragmentation through this pathway. We found that exposing H9C2 cells to an HG concentration decreased cell viability and increased cell apoptosis and caspase-3. Empagliflozin could reverse the apoptosis effect of HG stimulation on H9C2 cells. In addition, the HG condition caused mitochondria fragmentation, which was reduced by empagliflozin. The expression of mitochondria fission protein was upregulated, and fusion proteins were downregulated under HG stimulation. The expression of fission proteins was decreased under empagliflozin treatment. Increased calcium accumulation was observed under the HG condition, which was decreased by empagliflozin. The increased expression of ERK 1/2 under HG stimulation was also reversed by empagliflozin. Our study shows that empagliflozin could reverse the HG condition, causing a calcium-dependent activation of the ERK 1/2 pathway, which caused mitochondria fragmentation in H9C2 cells. Full article
(This article belongs to the Special Issue Molecular and Pathophysiological Insights into the Pleiotropic Role of SGLT2i)
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Review

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13 pages, 919 KiB  
Review
Sodium-Glucose Cotransporter 2 Inhibitor Therapy in Different Scenarios of Heart Failure: An Overview of the Current Literature
by Silvia Prosperi, Andrea D’Amato, Aurora Labbro Francia, Sara Monosilio, Claudia Cestiè, Stefanie Marek Iannucci, Lucrezia Netti, Danilo Angotti, Domenico Filomena, Marco Valerio Mariani, Vincenzo Myftari, Rosanna Germanò, Sara Cimino, Massimo Mancone, Roberto Badagliacca, Viviana Maestrini, Paolo Severino and Carmine Dario Vizza
Int. J. Mol. Sci. 2024, 25(21), 11458; https://doi.org/10.3390/ijms252111458 - 25 Oct 2024
Viewed by 570
Abstract
Heart failure (HF) is a complex syndrome that requires tailored and patient-centered treatment. Sodium-glucose cotransporter 2 inhibitors (SGLT2is) constitute one of the four pillars of the medical treatment of HF. However, the 2023 ESC guidelines treat HF as a single entity without making [...] Read more.
Heart failure (HF) is a complex syndrome that requires tailored and patient-centered treatment. Sodium-glucose cotransporter 2 inhibitors (SGLT2is) constitute one of the four pillars of the medical treatment of HF. However, the 2023 ESC guidelines treat HF as a single entity without making clear distinctions in phenotypes according to etiology. This creates a “gap in knowledge”, causing much debate about the applicability of these drugs in peculiar clinical settings that are etiological and/or predisposing clinical conditions for HF. Furthermore, considering the variety of etiologies and different pathophysiological backgrounds of HF, one might question whether the use of SGLT2is is equally beneficial in all types of HF and whether certain drug-related properties may be exploited in different contexts. For example, SGLT2is can improve the metabolic and inflammatory state, which is fundamental in ischemic heart disease. Anti-inflammatory power can also play a paramount role in myocarditis or cardiotoxicity, while improving the congestive state and reducing filling pressure may be even more fundamental in restrictive heart disease or advanced heart disease. This review aims to gather the evidence currently present in the literature concerning the advantages or the disadvantages of using these drugs in these particular clinical settings, with the goal being an optimized and highly personalized treatment for HF. Full article
(This article belongs to the Special Issue Molecular and Pathophysiological Insights into the Pleiotropic Role of SGLT2i)
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