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Metabolic Mechanisms of Cardiac Injury
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Metabolic Mechanisms of Cardiac Injury

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: 20 April 2025 | Viewed by 2858

Special Issue Editor

Dr. Magdalena Zabielska-Kaczorowska

E-Mail Website
Guest Editor
Department of Physiology, Medical University of Gdansk, Gdansk, Poland
Interests: heart; heart metabolism; ischemic heart disease; energy metabolism; atherosclerosis; purine metabolism; AMP deaminase; cardiac hypoxia; heart failure; cardiovascular pharmacology; heart metabolism modulation
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The hearts of adult mammals can hardly regenerate after cardiac injury, which is associated with the irreversible loss of viable cardiomyocytes. Myocardial injury leads to disturbed contractility of the remaining living myocardium, detrimental cardiac remodeling, and, as a result, heart failure. A focus on the changes in myocardial energy metabolism, including fatty acid, glucose, and amino acid metabolism, in cardiac physiological and pathological states is crucial. Metabolites are not only a source of energy but also become critical regulators of gene expression and epigenetic patterns, which may affect heart regeneration.

Understanding the metabolic mechanisms of cardiac injury is critical to the development of diagnostic, treatment, and preventive strategies in the cardiology field. It is essential to promote endogenous regeneration of the heart to improve the prognosis of patients with cardiac injury and to find effective therapeutic strategies for it. However, the metabolic pathways of cardiac damage and heart failure are still elusive, and novel metabolic defects and pathways remain to be identified for screening, molecular diagnosis, drug-target development, and personalized medicine.

This Special Issue focuses on the role of energy metabolism in cardiac injury, intending to shed light on strategies for manipulating heart metabolism and promoting heart repair after cardiac injury.

Dr. Magdalena A. Zabielska-Kaczorowska
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

  • heart metabolism
  • fatty acid metabolism
  • glucose metabolism
  • amino acid metabolism
  • metabolism regulation
  • mitochondria

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Published Papers (2 papers)

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Research

13 pages, 1033 KiB  
Article
Progranulin, sICAM-1, and sVCAM-1 May Predict an Increased Risk for Ventricular Arrhythmias in Patients with Systemic Sclerosis
by Veronika Sebestyén, Balázs Ratku, Dóra Ujvárosy, Hajnalka Lőrincz, Dóra Tari, Lilla Végh, Gyöngyike Majai, Sándor Somodi, Dénes Páll, Gabriella Szűcs, Mariann Harangi and Zoltán Szabó
Int. J. Mol. Sci. 2024, 25(13), 7380; https://doi.org/10.3390/ijms25137380 - 5 Jul 2024
Viewed by 851
Abstract
In systemic sclerosis (SSc), fibrosis of the myocardium along with ongoing autoimmune inflammation can alter the electric function of the cardiac myocytes, which may increase the risk for ventricular arrhythmias and sudden cardiac death. We analyzed the electrocardiographic (ECG) variables describing ventricular repolarization [...] Read more.
In systemic sclerosis (SSc), fibrosis of the myocardium along with ongoing autoimmune inflammation can alter the electric function of the cardiac myocytes, which may increase the risk for ventricular arrhythmias and sudden cardiac death. We analyzed the electrocardiographic (ECG) variables describing ventricular repolarization such as QT interval, QT dispersion (QTd), T wave peak-to-end interval (Tpe), and arrhythmogeneity index (AIX) of 26 patients with SSc and 36 healthy controls. Furthermore, echocardiographic and laboratory parameters were examined, with a focus on inflammatory proteins like C-reactive ptotein (CRP), soluble intracellular adhesion molecule-1 (sICAM-1), soluble vascular adhesion molecule-1 (sVCAM-1), and progranulin (PGRN). The CRP, sICAM-1, and sVCAM-1 levels were positively correlated with the length of the QT interval. Although the serum PGRN levels were not increased in the SSc group compared to the controls, in SSc patients, the PGRN levels were positively correlated with the QT interval and the AIX. According to our results, we conclude that there may be a potential association between autoimmune inflammation and the risk for ventricular arrhythmias in patients with SSc. We emphasize that the measurement of laboratory parameters of inflammatory activity including CRP, PGRN, sVCAM-1, and sICAM-1 could be helpful in the prediction of sudden cardiac death in patients with SSc. Full article
(This article belongs to the Special Issue Metabolic Mechanisms of Cardiac Injury)
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13 pages, 4113 KiB  
Article
TIGAR Deficiency Blunts Angiotensin-II-Induced Cardiac Hypertrophy in Mice
by Xiaochen He, Quinesha A. Williams, Aubrey C. Cantrell, Jessie Besanson, Heng Zeng and Jian-Xiong Chen
Int. J. Mol. Sci. 2024, 25(4), 2433; https://doi.org/10.3390/ijms25042433 - 19 Feb 2024
Viewed by 1551
Abstract
Hypertension is the key contributor to pathological cardiac hypertrophy. Growing evidence indicates that glucose metabolism plays an essential role in cardiac hypertrophy. TP53-induced glycolysis and apoptosis regulator (TIGAR) has been shown to regulate glucose metabolism in pressure overload-induced cardiac remodeling. In the present [...] Read more.
Hypertension is the key contributor to pathological cardiac hypertrophy. Growing evidence indicates that glucose metabolism plays an essential role in cardiac hypertrophy. TP53-induced glycolysis and apoptosis regulator (TIGAR) has been shown to regulate glucose metabolism in pressure overload-induced cardiac remodeling. In the present study, we investigated the role of TIGAR in cardiac remodeling during Angiotensin II (Ang-II)-induced hypertension. Wild-type (WT) and TIGAR knockout (KO) mice were infused with Angiotensin-II (Ang-II, 1 µg/kg/min) via mini-pump for four weeks. The blood pressure was similar between the WT and TIGAR KO mice. The Ang-II infusion resulted in a similar reduction of systolic function in both groups, as evidenced by the comparable decrease in LV ejection fraction and fractional shortening. The Ang-II infusion also increased the isovolumic relaxation time and myocardial performance index to the same extent in WT and TIGAR KO mice, suggesting the development of similar diastolic dysfunction. However, the knockout of TIGAR significantly attenuated hypertension-induced cardiac hypertrophy. This was associated with higher levels of fructose 2,6-bisphosphate, PFK-1, and Glut-4 in the TIGAR KO mice. Our present study suggests that TIGAR is involved in the control of glucose metabolism and glucose transporters by Ang-II and that knockout of TIGAR attenuates the development of maladaptive cardiac hypertrophy. Full article
(This article belongs to the Special Issue Metabolic Mechanisms of Cardiac Injury)
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