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Advances in Molecular Research of Diabetic Cardiomyopathy

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: 20 December 2024 | Viewed by 5920

Special Issue Editors


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Guest Editor

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Guest Editor
Department of Surgery, Dentistry, Pediatrics and Gynecology, Division of Cardiac Surgery, University of Verona, 37134 Verona, Italy
Interests: aortic valve calcification; myocardial ischemia–reperfusion injury; heart failure; heart transplanta-tion
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

This Special Issue will enclose a number of papers related to diabetic cardiomyopathy (DCM). DCM is the consequence of an altered glucose metabolism, leading to structural heart defects and altered activity. It is associated with oxidative stress, overactivation and expression of the renin angiotensin aldosterone system, abnormalities in intracellular calcium transport, mitochondrial dysfunction, and so on, but these mechanisms are not completely understood. To sum up, DCM is an independent complication of diabetes with a complex pathogenesis. There is no specific treatment so far, which mainly focuses on controlling blood sugar, lowering blood pressure and blood lipids, and improving lifestyles. Thus, this Special Issue will include research papers as well as reviews focusing on molecular studies highlighting the following:

  • Mechanisms of DCM development.
  • Therapeutic intervention, including possible clinical trials.
  • Stem cell-based approaches for intervention strategies against DCM.
  • Gene target therapy.

Dr. Giacomina Brunetti
Dr. Antonella Galeone
Guest Editors

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Keywords

  • diabetic cardiomyopathy
  • apoptosis
  • diabetes
  • myocardial fibrosis
  • stem cells
  • inflammation
  • therapeutic approaches

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Published Papers (3 papers)

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Review

14 pages, 1037 KiB  
Review
Diabetic Cardiomyopathy: Role of Cell Death, Exosomes, Fibrosis and Epicardial Adipose Tissue
by Antonella Galeone, Alessia Annicchiarico, Cinzia Buccoliero, Barbara Barile, Giovanni Battista Luciani, Francesco Onorati, Grazia Paola Nicchia and Giacomina Brunetti
Int. J. Mol. Sci. 2024, 25(17), 9481; https://doi.org/10.3390/ijms25179481 - 31 Aug 2024
Viewed by 1546
Abstract
Diabetic cardiomyopathy (DCM) represents one of the typical complications associated with diabetes. It has been described as anomalies in heart function and structure, with consequent high morbidity and mortality. DCM development can be described by two stages; the first is characterized by left [...] Read more.
Diabetic cardiomyopathy (DCM) represents one of the typical complications associated with diabetes. It has been described as anomalies in heart function and structure, with consequent high morbidity and mortality. DCM development can be described by two stages; the first is characterized by left ventricular hypertrophy and diastolic dysfunction, and the second by heart failure (HF) with systolic dysfunction. The proposed mechanisms involve cardiac inflammation, advanced glycation end products (AGEs) and angiotensin II. Furthermore, different studies have focused their attention on cardiomyocyte death through the different mechanisms of programmed cell death, such as apoptosis, autophagy, necrosis, pyroptosis and ferroptosis. Exosome release, adipose epicardial tissue and aquaporins affect DCM development. This review will focus on the description of the mechanisms involved in DCM progression and development. Full article
(This article belongs to the Special Issue Advances in Molecular Research of Diabetic Cardiomyopathy)
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14 pages, 1159 KiB  
Review
Acute Hyperglycemia-Induced Injury in Myocardial Infarction
by Martino Pepe, Francesco Addabbo, Annagrazia Cecere, Rocco Tritto, Gianluigi Napoli, Palma Luisa Nestola, Plinio Cirillo, Giuseppe Biondi-Zoccai, Salvatore Giordano and Marco Matteo Ciccone
Int. J. Mol. Sci. 2024, 25(15), 8504; https://doi.org/10.3390/ijms25158504 - 4 Aug 2024
Viewed by 2352
Abstract
Acute hyperglycemia is a transient increase in plasma glucose level (PGL) frequently observed in patients with ST-elevation myocardial infarction (STEMI). The aim of this review is to clarify the molecular mechanisms whereby acute hyperglycemia impacts coronary flow and myocardial perfusion in patients with [...] Read more.
Acute hyperglycemia is a transient increase in plasma glucose level (PGL) frequently observed in patients with ST-elevation myocardial infarction (STEMI). The aim of this review is to clarify the molecular mechanisms whereby acute hyperglycemia impacts coronary flow and myocardial perfusion in patients with acute myocardial infarction (AMI) and to discuss the consequent clinical and prognostic implications. We conducted a comprehensive literature review on the molecular causes of myocardial damage driven by acute hyperglycemia in the context of AMI. The negative impact of high PGL on admission recognizes a multifactorial etiology involving endothelial function, oxidative stress, production of leukocyte adhesion molecules, platelet aggregation, and activation of the coagulation cascade. The current evidence suggests that all these pathophysiological mechanisms compromise myocardial perfusion as a whole and not only in the culprit coronary artery. Acute hyperglycemia on admission, regardless of whether or not in the context of a diabetes mellitus history, could be, thus, identified as a predictor of worse myocardial reperfusion and poorer prognosis in patients with AMI. In order to reduce hyperglycemia-related complications, it seems rational to pursue in these patients an adequate and quick control of PGL, despite the best pharmacological treatment for acute hyperglycemia still remaining a matter of debate. Full article
(This article belongs to the Special Issue Advances in Molecular Research of Diabetic Cardiomyopathy)
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21 pages, 1602 KiB  
Review
Molecular Basis of Cardiomyopathies in Type 2 Diabetes
by Silvia Giardinelli, Giovanni Meliota, Donatella Mentino, Gabriele D’Amato and Maria Felicia Faienza
Int. J. Mol. Sci. 2024, 25(15), 8280; https://doi.org/10.3390/ijms25158280 - 29 Jul 2024
Viewed by 1631
Abstract
Diabetic cardiomyopathy (DbCM) is a common complication in individuals with type 2 diabetes mellitus (T2DM), and its exact pathogenesis is still debated. It was hypothesized that chronic hyperglycemia and insulin resistance activate critical cellular pathways that are responsible for numerous functional and anatomical [...] Read more.
Diabetic cardiomyopathy (DbCM) is a common complication in individuals with type 2 diabetes mellitus (T2DM), and its exact pathogenesis is still debated. It was hypothesized that chronic hyperglycemia and insulin resistance activate critical cellular pathways that are responsible for numerous functional and anatomical perturbations in the heart. Interstitial inflammation, oxidative stress, myocardial apoptosis, mitochondria dysfunction, defective cardiac metabolism, cardiac remodeling, hypertrophy and fibrosis with consequent impaired contractility are the most common mechanisms implicated. Epigenetic changes also have an emerging role in the regulation of these crucial pathways. The aim of this review was to highlight the increasing knowledge on the molecular mechanisms of DbCM and the new therapies targeting specific pathways. Full article
(This article belongs to the Special Issue Advances in Molecular Research of Diabetic Cardiomyopathy)
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