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Special Issue "Metabolic Therapies for Heart Failure"

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Endocrinology and Metabolism".

Deadline for manuscript submissions: 31 December 2021.

Special Issue Editor

Dr. Mathias Mericskay
E-Mail Website
Guest Editor
INSERM Research Unit on Signaling and Cardiovascular Pathophysiology, Paris-Saclay University, Châtenay-Malabry, France
Interests: heart failure; dilated cardiomyopathy; NAD signaling; cardiac bioenergetics; mitochondrial function

Special Issue Information

Dear Colleagues,

Heart failure (HF) is a debilitating syndrome associated with the inability of the cardiac pump to deliver enough oxygen and nutrients to the peripheral organs and is accompanied by a high risk of arrhythmia and sudden death. Strongly associated with age, vascular and metabolic comorbidities and sedentary way of life, HF prevalence is fated to rise with the aging of the world population. Currently, even with optimal treatment, mortality rates remain close to 40% at 5 years after prognosis. There is thus an urgent need for new approaches to halt or reverse the course of ventricular dysfunction leading to terminal HF.

This Special Issue focuses on recent developments in the field of metabolic therapies aimed at correcting the metabolic perturbations that characterize the failing heart. These perturbations include inflexibility in the use of energy substrates, severe mitochondrial dysfunction and increased oxidative stress. They all have major consequences not only for cardiac contractility and ion homeostasis but also for cardiac cell survival, intracellular signaling and epigenetic regulation of gene expression. Hence, metabolic therapies can potentially have a broad impact on cardiac physiology, and a combination of many different types of expertise is required to assess their efficacy and safety for the treatment of patients with heart failure.

We warmly welcome the submission of original papers and reviews on new therapeutic strategies addressing these key issues.

Dr. Mathias Mericskay
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 papers will be 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

  • Heart failure
  • Metabolic therapy
  • Nutrition therapy
  • Energy metabolism
  • Mitochondrial function
  • Oxidative stress
  • Autophagy
  • Coenzyme metabolism
  • Glucose metabolism
  • Fatty acid metabolism
  • Ketone body metabolism
  • Insulin signaling
  • Energy-sensing signaling pathways
  • Redox-sensing signaling pathways

Published Papers (3 papers)

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Communication
Implications of a Soy-Based Diet for Animal Models
Int. J. Mol. Sci. 2021, 22(2), 774; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22020774 - 14 Jan 2021
Cited by 1 | Viewed by 469
Abstract
The use of animal models in fundamental or pre-clinical research remains an absolute requirement for understanding human pathologies and developing new drugs. In order to transpose these results into clinical practice, many parameters must be taken into account to limit bias. Attention has [...] Read more.
The use of animal models in fundamental or pre-clinical research remains an absolute requirement for understanding human pathologies and developing new drugs. In order to transpose these results into clinical practice, many parameters must be taken into account to limit bias. Attention has recently been focused on the sex, age or even strain of each animal, but the impact of diet has been largely neglected. Soy, which is commonly used in the diet in varying quantities can affect their physiology. In order to assess whether the presence of soy can impact the obtained results, we studied the impact of a soy-based diet versus a soy-free diet, on diastolic function in a rat model based on transgenic overexpression of the β3-adrenergic receptors in the endothelium and characterized by the appearance of diastolic dysfunction with age. Our results show that the onset of diastolic dysfunction is only observed in transgenic male rats fed with a soy-free diet in the long term. Our study highlights the importance of the diet’s choice in the study design process, especially regarding the proportion of soy, to correctly interpret the outcome as low-cost diets are more likely to be highly concentrated in soy. Full article
(This article belongs to the Special Issue Metabolic Therapies for Heart Failure)
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Review

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Review
Targeting Adrenergic Receptors in Metabolic Therapies for Heart Failure
Int. J. Mol. Sci. 2021, 22(11), 5783; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22115783 - 28 May 2021
Viewed by 692
Abstract
The heart has a reduced capacity to generate sufficient energy when failing, resulting in an energy-starved condition with diminished functions. Studies have identified numerous changes in metabolic pathways in the failing heart that result in reduced oxidation of both glucose and fatty acid [...] Read more.
The heart has a reduced capacity to generate sufficient energy when failing, resulting in an energy-starved condition with diminished functions. Studies have identified numerous changes in metabolic pathways in the failing heart that result in reduced oxidation of both glucose and fatty acid substrates, defects in mitochondrial functions and oxidative phosphorylation, and inefficient substrate utilization for the ATP that is produced. Recent early-phase clinical studies indicate that inhibitors of fatty acid oxidation and antioxidants that target the mitochondria may improve heart function during failure by increasing compensatory glucose oxidation. Adrenergic receptors (α1 and β) are a key sympathetic nervous system regulator that controls cardiac function. β-AR blockers are an established treatment for heart failure and α1A-AR agonists have potential therapeutic benefit. Besides regulating inotropy and chronotropy, α1- and β-adrenergic receptors also regulate metabolic functions in the heart that underlie many cardiac benefits. This review will highlight recent studies that describe how adrenergic receptor-mediated metabolic pathways may be able to restore cardiac energetics to non-failing levels that may offer promising therapeutic strategies. Full article
(This article belongs to the Special Issue Metabolic Therapies for Heart Failure)
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Review
Nutraceutical, Dietary, and Lifestyle Options for Prevention and Treatment of Ventricular Hypertrophy and Heart Failure
Int. J. Mol. Sci. 2021, 22(7), 3321; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22073321 - 24 Mar 2021
Cited by 1 | Viewed by 1109
Abstract
Although well documented drug therapies are available for the management of ventricular hypertrophy (VH) and heart failure (HF), most patients nonetheless experience a downhill course, and further therapeutic measures are needed. Nutraceutical, dietary, and lifestyle measures may have particular merit in this regard, [...] Read more.
Although well documented drug therapies are available for the management of ventricular hypertrophy (VH) and heart failure (HF), most patients nonetheless experience a downhill course, and further therapeutic measures are needed. Nutraceutical, dietary, and lifestyle measures may have particular merit in this regard, as they are currently available, relatively safe and inexpensive, and can lend themselves to primary prevention as well. A consideration of the pathogenic mechanisms underlying the VH/HF syndrome suggests that measures which control oxidative and endoplasmic reticulum (ER) stress, that support effective nitric oxide and hydrogen sulfide bioactivity, that prevent a reduction in cardiomyocyte pH, and that boost the production of protective hormones, such as fibroblast growth factor 21 (FGF21), while suppressing fibroblast growth factor 23 (FGF23) and marinobufagenin, may have utility for preventing and controlling this syndrome. Agents considered in this essay include phycocyanobilin, N-acetylcysteine, lipoic acid, ferulic acid, zinc, selenium, ubiquinol, astaxanthin, melatonin, tauroursodeoxycholic acid, berberine, citrulline, high-dose folate, cocoa flavanols, hawthorn extract, dietary nitrate, high-dose biotin, soy isoflavones, taurine, carnitine, magnesium orotate, EPA-rich fish oil, glycine, and copper. The potential advantages of whole-food plant-based diets, moderation in salt intake, avoidance of phosphate additives, and regular exercise training and sauna sessions are also discussed. There should be considerable scope for the development of functional foods and supplements which make it more convenient and affordable for patients to consume complementary combinations of the agents discussed here. Research Strategy: Key word searching of PubMed was employed to locate the research papers whose findings are cited in this essay. Full article
(This article belongs to the Special Issue Metabolic Therapies for Heart Failure)
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