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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: 30 June 2024 | Viewed by 946

Special Issue Editor


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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
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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

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Keywords

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

Published Papers (1 paper)

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Research

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 709
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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