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Metabolic Regulation in the Development of Cardiovascular Disease and Heart Failure, 2nd Edition

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: closed (20 September 2024) | Viewed by 8305

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Guest Editor
Cardiology Unit, Department of Medical and Surgical Sciences, University of Foggia, Viale Luigi Pinto 1, 71122 Foggia, Italy
Interests: cardiology; heart failure; cardiac arrest
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Special Issue Information

Dear Colleagues,

This Special Issue is the continuation of our previous Special Issue, entitled "Metabolic Regulation in the Development of Cardiovascular Disease and Heart Failure".

Metabolic regulation is strongly related to the development of cardiovascular diseases and heart failure. Different metabolic diseases can predispose the patient to the occurrence of systolic and diastolic dysfunction and, consequently, to heart failure. Among those, impaired glucose metabolism is the metabolic condition most commonly associated with a greater incidence of both coronary artery disease and heart failure. Novel classes of hypoglycemic drugs, such as type 2 sodium-glucose cotransporter inhibitors (SGLT2i) or GLP-1 agonists, have been demonstrated to exert greater cardio- and nefro-protection effects. In particular, the use of SGLT2i reduce the risk of heart failure occurrence and of heart failure progression.

However, metabolic regulation in cardiovascular disease and heart failure is complex, and its different stages are characterized by differences in metabolic and hormonal status. In patients with advanced heart failure, the dysregulation of metabolism is associated with a greater catabolic status due to a number of pathophysiological mechanisms. These are responsible for paradoxical epidemiology and cardiac cachexia. The study of the metabolic therapeutic approaches used to treat heart failure patients at different stages is a challenging field of research. This Special Issue aims to present a collection of reviews and original papers that better clarify a range of topics, from the pathophysiological, diagnostic, and therapeutic aspects of metabolic regulation related to the risk of cardiovascular disease occurrence through to the onset and progression of heart failure.

Dr. Massimo Iacoviello
Guest Editor

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Keywords

  • diabetes
  • metabolism
  • dyslipidemia
  • cardiovascular disease
  • heart failure
  • diagnosis
  • prognosis
  • therapy

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Published Papers (3 papers)

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Review

22 pages, 2436 KiB  
Review
The Role of Programmed Types of Cell Death in Pathogenesis of Heart Failure with Preserved Ejection Fraction
by Jan Jankowski, Kamil Oskar Kozub, Marcin Kleibert, Katarzyna Camlet, Klaudia Kleibert and Agnieszka Cudnoch-Jędrzejewska
Int. J. Mol. Sci. 2024, 25(18), 9921; https://doi.org/10.3390/ijms25189921 - 14 Sep 2024
Viewed by 1365
Abstract
Heart failure with preserved ejection fraction (HFpEF) is a condition that develops in the course of many diseases and conditions, and its pathophysiology is still not well understood, but the involvement of programmed types of cell death in the development of this type [...] Read more.
Heart failure with preserved ejection fraction (HFpEF) is a condition that develops in the course of many diseases and conditions, and its pathophysiology is still not well understood, but the involvement of programmed types of cell death in the development of this type of heart failure is becoming increasingly certain. In addition, drugs already widely used in clinical practice, with a good safety profile and efficacy demonstrated in large-group clinical trials, seem to be exerting their beneficial effects on cardiovascular health. Perhaps new drugs that reduce the susceptibility of cells to programmed types of cell death are under investigation and may improve the prognosis of patients with HFpEF. In this article, we summarize the current knowledge about the pathogenesis of HFpEF and the role of programmed types of cell death in its development. Additionally, we have described the future directions of research that may lead to the improvement of a patient’s prognosis and potential treatment. Full article
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28 pages, 5536 KiB  
Review
Generation and Accumulation of Various Advanced Glycation End-Products in Cardiomyocytes May Induce Cardiovascular Disease
by Takanobu Takata, Shinya Inoue, Togen Masauji, Katsuhito Miyazawa and Yoshiharu Motoo
Int. J. Mol. Sci. 2024, 25(13), 7319; https://doi.org/10.3390/ijms25137319 - 3 Jul 2024
Cited by 3 | Viewed by 1777
Abstract
Cardiomyocyte dysfunction and cardiovascular diseases (CVDs) can be classified as ischemic or non-ischemic. We consider the induction of cardiac tissue dysfunction by intracellular advanced glycation end-products (AGEs) in cardiomyocytes as a novel type of non-ischemic CVD. Various types of AGEs can be generated [...] Read more.
Cardiomyocyte dysfunction and cardiovascular diseases (CVDs) can be classified as ischemic or non-ischemic. We consider the induction of cardiac tissue dysfunction by intracellular advanced glycation end-products (AGEs) in cardiomyocytes as a novel type of non-ischemic CVD. Various types of AGEs can be generated from saccharides (glucose and fructose) and their intermediate/non-enzymatic reaction byproducts. Recently, certain types of AGEs (Nε-carboxymethyl-lycine [CML], 2-ammnonio-6-[4-(hydroxymetyl)-3-oxidopyridinium-1-yl]-hexanoate-lysine [4-hydroxymethyl-OP-lysine, hydroxymethyl-OP-lysine], and Nδ-(5-hydro-5-methyl-4-imidazolone-2-yl)-ornithine [MG-H1]) were identified and quantified in the ryanodine receptor 2 (RyR2) and F-actin–tropomyosin filament in the cardiomyocytes of mice or patients with diabetes and/or heart failure. Under these conditions, the excessive leakage of Ca2+ from glycated RyR2 and reduced contractile force from glycated F-actin–tropomyosin filaments induce cardiomyocyte dysfunction. CVDs are included in lifestyle-related diseases (LSRDs), which ancient people recognized and prevented using traditional medicines (e.g., Kampo medicines). Various natural compounds, such as quercetin, curcumin, and epigallocatechin-3-gallate, in these drugs can inhibit the generation of intracellular AGEs through mechanisms such as the carbonyl trap effect and glyoxalase 1 activation, potentially preventing CVDs caused by intracellular AGEs, such as CML, hydroxymethyl-OP, and MG-H1. These investigations showed that bioactive herbal extracts obtained from traditional medicine treatments may contain compounds that prevent CVDs. Full article
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16 pages, 1538 KiB  
Review
Renal Oxygen Demand and Nephron Function: Is Glucose a Friend or Foe?
by Edoardo Gronda, Alberto Palazzuoli, Massimo Iacoviello, Manuela Benevenuto, Domenico Gabrielli and Arduino Arduini
Int. J. Mol. Sci. 2023, 24(12), 9957; https://doi.org/10.3390/ijms24129957 - 9 Jun 2023
Cited by 2 | Viewed by 4219
Abstract
The kidneys and heart work together to balance the body’s circulation, and although their physiology is based on strict inter dependence, their performance fulfills different aims. While the heart can rapidly increase its own oxygen consumption to comply with the wide changes in [...] Read more.
The kidneys and heart work together to balance the body’s circulation, and although their physiology is based on strict inter dependence, their performance fulfills different aims. While the heart can rapidly increase its own oxygen consumption to comply with the wide changes in metabolic demand linked to body function, the kidneys physiology are primarily designed to maintain a stable metabolic rate and have a limited capacity to cope with any steep increase in renal metabolism. In the kidneys, glomerular population filters a large amount of blood and the tubular system has been programmed to reabsorb 99% of filtrate by reabsorbing sodium together with other filtered substances, including all glucose molecules. Glucose reabsorption involves the sodium–glucose cotransporters SGLT2 and SGLT1 on the apical membrane in the proximal tubular section; it also enhances bicarbonate formation so as to preserve the acid–base balance. The complex work of reabsorption in the kidney is the main factor in renal oxygen consumption; analysis of the renal glucose transport in disease states provides a better understanding of the renal physiology changes that occur when clinical conditions alter the neurohormonal response leading to an increase in glomerular filtration pressure. In this circumstance, glomerular hyperfiltration occurs, imposing a higher metabolic demand on kidney physiology and causing progressive renal impairment. Albumin urination is the warning signal of renal engagement over exertion and most frequently heralds heart failure development, regardless of disease etiology. The review analyzes the mechanisms linked to renal oxygen consumption, focusing on sodium–glucose management. Full article
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