Metabolic Remodeling in Heart Failure: Cause or Consequence?

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cells of the Cardiovascular System".

Deadline for manuscript submissions: closed (1 December 2022) | Viewed by 3262

Special Issue Editors


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Guest Editor
Division of Cardiology, Department of Medicine, School of Medicine, Case Western Reserve University, Cleveland, OH, USA
Interests: molecular cardiology; mitochondrial biology; transcriptional regulation.

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Guest Editor
Division of Cardiovascular Medicine, Department of Internal Medicine, School of Medicine, Toho University, Tokyo, Japan
Interests: Ischemic heart disease

Special Issue Information

Dear Colleagues,

We are pleased to invite you to submit your work to this Special Issue of Cells on metabolic remodeling in heart failure.

There is no doubt that heart function is closely associated with metabolism at both the myocardial and systemic levels. Despite its high-energy demand, the heart contains relatively low ATP reserves, and thus, a strict control of myocardial metabolism is a requisite to ensure a continual supply of energy. Not surprisingly, heart failure is highly associated with energy insufficiency and metabolic remodeling in the myocardium. Conversely, heart failure causes reduced blood perfusion to the body that may alter peripheral metabolism due to tissue hypoxia, acidification, electrolyte disturbances or substrate deprivation. Finally, abnormalities in whole-body metabolism, such as hyperglycemia and hyperlipidemia, are well-known risk factors of heart failure.

However, many issues still remain debatable. For example, is metabolic remodeling a cause or consequence of heart failure, or an interplay of the two sides? What is the precise cause of myocardial metabolic dysfunction in the non-ischemic settings and in the chronic remodeling phase post-MI? What are the molecular mechanisms underlying metabolic remodeling in the myocardium of chronic heart failure? As heart failure is largely a disease of the elderly, how does aging affect or remodel metabolism? How can we improve heart failure treatments by targeting the metabolic pathways? This Special Issue aims to discuss the above questions and other related topics.

In this Special Issue, original research articles and reviews are welcome. Research areas may include (but are not limited to) the following: animal heart failure studies (with focus on metabolism), molecular and pathological studies of clinic heart failure, cellular metabolism, mitochondrial biology, autophagy/mitophagy, translational studies on targeting metabolism in heart failure, etc.

We look forward to receiving your contributions. 

Dr. Xudong Liao
Dr. Ippei Watanabe
Guest Editors

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Keywords

  • heart failure
  • cardiomyopathy
  • metabolism
  • remodeling

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Published Papers (1 paper)

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Research

18 pages, 7250 KiB  
Article
Alterations of Lipid Metabolism in the Heart in Spontaneously Hypertensive Rats Precedes Left Ventricular Hypertrophy and Cardiac Dysfunction
by Tomasz K. Bednarski, Monika K. Duda and Pawel Dobrzyn
Cells 2022, 11(19), 3032; https://doi.org/10.3390/cells11193032 - 27 Sep 2022
Cited by 14 | Viewed by 2903
Abstract
Disturbances in cardiac lipid metabolism are associated with the development of cardiac hypertrophy and heart failure. Spontaneously hypertensive rats (SHRs), a genetic model of primary hypertension and pathological left ventricular (LV) hypertrophy, have high levels of diacylglycerols in cardiomyocytes early in development. However, [...] Read more.
Disturbances in cardiac lipid metabolism are associated with the development of cardiac hypertrophy and heart failure. Spontaneously hypertensive rats (SHRs), a genetic model of primary hypertension and pathological left ventricular (LV) hypertrophy, have high levels of diacylglycerols in cardiomyocytes early in development. However, the exact effect of lipids and pathways that are involved in their metabolism on the development of cardiac dysfunction in SHRs is unknown. Therefore, we used SHRs and Wistar Kyoto (WKY) rats at 6 and 18 weeks of age to analyze the impact of perturbations of processes that are involved in lipid synthesis and degradation in the development of LV hypertrophy in SHRs with age. Triglyceride levels were higher, whereas free fatty acid (FA) content was lower in the LV in SHRs compared with WKY rats. The expression of de novo FA synthesis proteins was lower in cardiomyocytes in SHRs compared with corresponding WKY controls. The higher expression of genes that are involved in TG synthesis in 6-week-old SHRs may explain the higher TG content in these rats. Adenosine monophosphate-activated protein kinase phosphorylation and peroxisome proliferator-activated receptor α protein content were lower in cardiomyocytes in 18-week-old SHRs, suggesting a lower rate of β-oxidation. The decreased protein content of α/β-hydrolase domain-containing 5, adipose triglyceride lipase (ATGL) activator, and increased content of G0/G1 switch protein 2, ATGL inhibitor, indicating a lower rate of lipolysis in the heart in SHRs. In conclusion, the present study showed that the development of LV hypertrophy and myocardial dysfunction in SHRs is associated with triglyceride accumulation, attributable to a lower rate of lipolysis and β-oxidation in cardiomyocytes. Full article
(This article belongs to the Special Issue Metabolic Remodeling in Heart Failure: Cause or Consequence?)
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