Search for Articles:
Title / Keyword
Author / Affiliation / Email
Journal
Article Type
 
 
Advanced Search
 
Section
Special Issue
Volume
Issue
Number
Page
 
2.7
3.2
Journals
Life
Special Issues
Recent Advances in Diabetic Cardiomyopathies
share announcement

Recent Advances in Diabetic Cardiomyopathies

A special issue of Life (ISSN 2075-1729). This special issue belongs to the section "Physiology and Pathology".

Deadline for manuscript submissions: closed (31 December 2022) | Viewed by 4243

Special Issue Editor

Prof. Dr. Ernest Adeghate

E-Mail Website
Guest Editor
College of Medicine and Health Sciences, UAE University, Al Ain P.O. Box 15551, United Arab Emirates
Interests: anatomy; diabetes; metabolism; cardiovascular research; neuroendocrinology
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Current reports show that diabetes mellitus (DM) currently affects more than 537 million people worldwide. The prevalence of DM is projected to reach 783 million in adults aged between 20 and 79 years old by the year 2045. In 2019, the direct and indirect cost of managing DM and its complications was estimated to be USD 760 billion. All of these show the magnitude of the burden of DM and its complication on the global healthcare system. DM is a major risk factor for cardiovascular diseases such as diabetic cardiomyopathy. Diabetic cardiomyopathy is twice as common in people suffering from DM compared to non-diabetics. This risk factor increases exponentially even with small elevations in blood glucose level. It is also well known that the major causative factor in the development of diabetic cardiomyopathy is hyperglycemia-induced oxidative stress, which induces both biochemical as well as morphological alterations in the myocardium. The consequence of these changes in the myocardium may lead to severe morbidity that can result in fatal heart failure. There are many areas of the etiopathological mechanisms, pharmacotherapy, diagnosis, and management of diabetic cardiomyopathy that need to be clarified. In addition, new molecular pathways involved in the development of diabetic cardiomyopathy would need to be elucidated.

This Special Issue on diabetic cardiomyopathy aims to address the most recent and novel advances on the pathophysiology, pathology, risk factors, pharmacotherapy, and management protocols for the prevention and management of diabetic cardiomyopathy.  All researchers working in the field of diabetic cardiomyopathy, including molecular and cellular biologists, physiologists, pathologists, pharmacologists, clinicians, and other colleagues, are encouraged to submit their work. Original articles, reviews, and clinical trials are welcome.

Prof. Dr. Ernest Adeghate
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Life is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • diabetic cardiomyopathy
  • risk factors for the development of diabetic cardiomyopathy
  • diabetes-induced heart failure
  • metabolic syndrome and the heart
  • molecular mechanisms underlying diabetic cardiomyopathy
  • pharmacological treatment of diabetic cardiomyopathy
  • lifestyle modifications in the management of diabetic cardiomyopathy
  • diet and antioxidants in the management of diabetic cardiomyopathy
  • novel therapies for diabetic cardiomyopathy

Published Papers (2 papers)

Download All Papers
Order results
Result details
Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:

Research

Jump to: Review

20 pages, 5075 KiB  
Article
Embryonic Hyperglycemia Disrupts Myocardial Growth, Morphological Development, and Cellular Organization: An In Vivo Experimental Study
by Ricardo Jaime-Cruz, Concepción Sánchez-Gómez, Laura Villavicencio-Guzmán, Roberto Lazzarini-Lechuga, Carlos César Patiño-Morales, Mario García-Lorenzana, Tania Cristina Ramírez-Fuentes and Marcela Salazar-García
Life 2023, 13(3), 768; https://doi.org/10.3390/life13030768 - 13 Mar 2023
Cited by 2 | Viewed by 1788
Abstract
Hyperglycemia during gestation can disrupt fetal heart development and increase postnatal cardiovascular disease risk. It is therefore imperative to identify early biomarkers of hyperglycemia during gestation-induced fetal heart damage and elucidate the underlying molecular pathomechanisms. Clinical investigations of diabetic adults with heart dysfunction [...] Read more.
Hyperglycemia during gestation can disrupt fetal heart development and increase postnatal cardiovascular disease risk. It is therefore imperative to identify early biomarkers of hyperglycemia during gestation-induced fetal heart damage and elucidate the underlying molecular pathomechanisms. Clinical investigations of diabetic adults with heart dysfunction and transgenic mouse studies have revealed that overexpression or increased expression of TNNI3K, a heart-specific kinase that binds troponin cardiac I, may contribute to abnormal cardiac remodeling, ventricular hypertrophy, and heart failure. Optimal heart function also depends on the precise organization of contractile and excitable tissues conferred by intercellular occlusive, adherent, and communicating junctions. The current study evaluated changes in embryonic heart development and the expression levels of sarcomeric proteins (troponin I, desmin, and TNNI3K), junctional proteins, glucose transporter-1, and Ki-67 under fetal hyperglycemia. Stage 22HH Gallus domesticus embryos were randomly divided into two groups: a hyperglycemia (HG) group, in which individual embryos were injected with 30 mmol/L glucose solution every 24 h for 10 days, and a no-treatment (NT) control group, in which individual embryos were injected with physiological saline every 24 h for 10 days (stage 36HH). Embryonic blood glucose, height, and weight, as well as heart size, were measured periodically during treatment, followed by histopathological analysis and estimation of sarcomeric and junctional protein expression by western blotting and immunostaining. Hyperglycemic embryos demonstrated delayed heart maturation, with histopathological analysis revealing reduced left and right ventricular wall thickness (−39% and −35% vs. NT). Immunoexpression levels of TNNI3K and troponin 1 increased (by 37% and 39%, respectively), and desmin immunofluorescence reduced (by 23%). Embryo-fetal hyperglycemia may trigger an increase in the expression levels of TNNI3K and troponin I, as well as dysfunction of occlusive and adherent junctions, ultimately inducing abnormal cardiac remodeling. Full article
(This article belongs to the Special Issue Recent Advances in Diabetic Cardiomyopathies)
►▼ Show Figures

Figure 1

Review

Jump to: Research

16 pages, 814 KiB  
Review
The Role of Renin–Angiotensin System in Diabetic Cardiomyopathy: A Narrative Review
by João Pedro Thimotheo Batista, André Oliveira Vilela de Faria, Thomas Felipe Silva Ribeiro and Ana Cristina Simões e Silva
Life 2023, 13(7), 1598; https://doi.org/10.3390/life13071598 - 21 Jul 2023
Cited by 2 | Viewed by 2030
Abstract
Diabetic cardiomyopathy refers to myocardial dysfunction in type 2 diabetes, but without the traditional cardiovascular risk factors or overt clinical atherosclerosis and valvular disease. The activation of the renin–angiotensin system (RAS), oxidative stress, lipotoxicity, maladaptive immune responses, imbalanced mitochondrial dynamics, impaired myocyte autophagy, [...] Read more.
Diabetic cardiomyopathy refers to myocardial dysfunction in type 2 diabetes, but without the traditional cardiovascular risk factors or overt clinical atherosclerosis and valvular disease. The activation of the renin–angiotensin system (RAS), oxidative stress, lipotoxicity, maladaptive immune responses, imbalanced mitochondrial dynamics, impaired myocyte autophagy, increased myocyte apoptosis, and fibrosis contribute to diabetic cardiomyopathy. This review summarizes the studies that address the link between cardiomyopathy and the RAS in humans and presents proposed pathophysiological mechanisms underlying this association. The RAS plays an important role in the development and progression of diabetic cardiomyopathy. The over-activation of the classical RAS axis in diabetes leads to the increased production of angiotensin (Ang) II, angiotensin type 1 receptor activation, and aldosterone release, contributing to increased oxidative stress, fibrosis, and cardiac remodeling. In contrast, Ang-(1-7) suppresses oxidative stress, inhibits tissue fibrosis, and prevents extensive cardiac remodeling. Angiotensin-converting-enzyme (ACE) inhibitors and angiotensin receptor blockers improve heart functioning and reduce the occurrence of diabetic cardiomyopathy. Experimental studies also show beneficial effects for Ang-(1-7) and angiotensin-converting enzyme 2 infusion in improving heart functioning and tissue injury. Further research is necessary to fully understand the pathophysiology of diabetic cardiomyopathy and to translate experimental findings into clinical practice. Full article
(This article belongs to the Special Issue Recent Advances in Diabetic Cardiomyopathies)
►▼ Show Figures

Figure 1

Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:
 
Displaying articles 1-2
Back to TopTop