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Cardiovascular Disease and Myocardial Metabolism
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Cardiovascular Disease and Myocardial Metabolism

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 (30 September 2023) | Viewed by 2235

Special Issue Editor

Dr. John A. St. Cyr

E-Mail Website
Guest Editor
Regulatory & Clinical Research Institute, University of Minnesota, Minneapolis, MN 55455, USA
Interests: cardiovascular surgery; congenital heart disease; heart failure; myocardial metabolism

Special Issue Information

Dear Colleagues,

Cardiovascular disease still ranks as the leading cause of death worldwide. Every human cell requires adequate levels of high energy phosphates, such as Adenosine Triphosphate (ATP), to maintain cellular integrity and function. Normally, this supply and demand relationship is maintained; however, during stressful conditions and in diseases, such as cardiovascular disease, a mismatch is found, where supply and demand is not satisfied. Numerous cardiovascular studies have shown that there is a clear relationship between myocardial cellular energy levels and functional status. Myocardial ischemia and ischemic heart failure have demonstrated a decrease in energy molecules, which is reflected in alterations in intracellular reactions and in cellular function. Because of this observed deficiency in cellular energy during myocardial ischemia, research over decades has explored ways in which to replenish this energy deficiency; and thereby, maintain cellular integrity and function. The current special issue of the International Journal of Molecular Sciences is dedicated to the importance of myocardial metabolism in cardiovascular diseases.

Dr. John A. St. Cyr
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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

  • cardiovascular disease
  • metabolism
  • myocardial energy
  • myocardial function

Published Papers (1 paper)

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Research

18 pages, 4590 KiB  
Article
Hypoxia-Inducible Factor 1-Alpha and Glucose Metabolism during Cardiac Remodeling Progression from Hypertrophy to Heart Failure
by Paula Grippa Sant’Ana, Loreta Casquel de Tomasi, Gilson Masahiro Murata, Danielle Fernandes Vileigas, Gustavo Augusto Ferreira Mota, Sérgio Luiz Borges de Souza, Vitor Loureiro Silva, Livia Paschoalino de Campos, Katashi Okoshi, Carlos Roberto Padovani and Antonio Carlos Cicogna
Int. J. Mol. Sci. 2023, 24(7), 6201; https://doi.org/10.3390/ijms24076201 - 25 Mar 2023
Cited by 8 | Viewed by 1911
Abstract
In pathological cardiac hypertrophy, the heart is more dependent on glucose than fatty acids. This shift in energy metabolism occurs due to several factors, including the oxygen deficit, which activates hypoxia-inducible factor-1α (HIF-1α), a critical molecule related to glucose metabolism. However, there are [...] Read more.
In pathological cardiac hypertrophy, the heart is more dependent on glucose than fatty acids. This shift in energy metabolism occurs due to several factors, including the oxygen deficit, which activates hypoxia-inducible factor-1α (HIF-1α), a critical molecule related to glucose metabolism. However, there are gaps regarding the behavior of key proteins in the glycolytic pathway and HIF-1α during the transition from hypertrophy to heart failure (HF). This study assesses the hypothesis that there is an early change and enhancement of HIF-1α and the glycolytic pathway, as well as an association between them during cardiac remodeling. Sham and aortic stenosis Wistar rats were analyzed at 2, 6, and 18 weeks and in HF (n = 10–18). Cardiac structure and function were investigated by echocardiogram. Myocardial glycolysis, the aerobic and anaerobic pathways and glycogen were analyzed by enzymatic assay, Western blot, and enzyme-linked immunosorbent assay (ELISA). The following were observed: increased left ventricular hypertrophy; early diastolic function change and severe systolic and diastolic dysfunction in HF; increased HIF-1α in the 2nd week and in HF; precocious alteration and intensification of glycolysis with a shift to anaerobic metabolism from the 6th week onwards; association between HIF-1α, glycolysis, and the anaerobic pathway. Our hypothesis was confirmed as there was an early change and intensification in glucose metabolism, alteration in HIF-1α, and an association between data during the progression from hypertrophy to heart failure. Full article
(This article belongs to the Special Issue Cardiovascular Disease and Myocardial Metabolism)
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