Metabolites in Cardio-Metabolic Disease: Unravelling New Markers and Mechanisms Volume 2

A special issue of Metabolites (ISSN 2218-1989). This special issue belongs to the section "Integrative Metabolomics".

Deadline for manuscript submissions: closed (15 April 2021) | Viewed by 3693

Special Issue Editors


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Guest Editor
Northern Clinical School, Kolling Institute of Medical Research, Faculty of Medicine and Health, St Leonards, Australia
Interests: coronary atherosclerosis; inflammation and oxidative stress in the heart and blood vessel; Clinical trials
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Guest Editor
Charles Perkins Centre, Camperdown, The University of Sydney, Sydney 2006, Australia
Interests: metabolites; cardiac metabolism; atherosclerosis; heart failure; diabetes
Special Issues, Collections and Topics in MDPI journals

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Guest Editor
Cardiovascular Discovery Group, Kolling Institute, University of Sydney, Sydney, NSW 2006, Australia
Interests: heart failure

Special Issue Information

Dear Colleagues,

Recent developments in technology platforms, including nuclear magnetic resonance spectroscopy and mass spectrometry, combined with advances in computational bioinformatics provide opportunities for unravelling completely unexpected mechanisms and new markers of disease risk. Such approaches are ideal tools for breakthrough discoveries in complex diseases typified by atherosclerosis, cardiomyopathy, and metabolic syndrome. Here we call for manuscripts addressing the current challenges of, and exploring opportunities for, the application of metabolomic studies in the cardiovascular field.

This Special Issue will cover recent advances and methodological limitations, as well as the clinical implications. Reviews and perspectives as well as original data are welcome.

Prof. Dr. Gemma Figtree
Dr. John O'Sullivan
Dr. Steve Vernon
Guest Editors

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Published Papers (1 paper)

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Research

15 pages, 2557 KiB  
Article
Metabolic Signature of Arrhythmogenic Cardiomyopathy
by Chiara Volani, Johannes Rainer, Vinicius Veri Hernandes, Viviana Meraviglia, Peter Paul Pramstaller, Sigurður Vidir Smárason, Giulio Pompilio, Michela Casella, Elena Sommariva, Giuseppe Paglia and Alessandra Rossini
Metabolites 2021, 11(4), 195; https://doi.org/10.3390/metabo11040195 - 25 Mar 2021
Cited by 7 | Viewed by 3220
Abstract
Arrhythmogenic cardiomyopathy (ACM) is a genetic-based cardiac disease accompanied by severe ventricular arrhythmias and a progressive substitution of the myocardium with fibro-fatty tissue. ACM is often associated with sudden cardiac death. Due to the reduced penetrance and variable expressivity, the presence of a [...] Read more.
Arrhythmogenic cardiomyopathy (ACM) is a genetic-based cardiac disease accompanied by severe ventricular arrhythmias and a progressive substitution of the myocardium with fibro-fatty tissue. ACM is often associated with sudden cardiac death. Due to the reduced penetrance and variable expressivity, the presence of a genetic defect is not conclusive, thus complicating the diagnosis of ACM. Recent studies on human induced pluripotent stem cells-derived cardiomyocytes (hiPSC-CMs) obtained from ACM individuals showed a dysregulated metabolic status, leading to the hypothesis that ACM pathology is characterized by an impairment in the energy metabolism. However, despite efforts having been made for the identification of ACM specific biomarkers, there is still a substantial lack of information regarding the whole metabolomic profile of ACM patients. The aim of the present study was to investigate the metabolic profiles of ACM patients compared to healthy controls (CTRLs). The targeted Biocrates AbsoluteIDQ® p180 assay was used on plasma samples. Our analysis showed that ACM patients have a different metabolome compared to CTRLs, and that the pathways mainly affected include tryptophan metabolism, arginine and proline metabolism and beta oxidation of fatty acids. Altogether, our data indicated that the plasma metabolomes of arrhythmogenic cardiomyopathy patients show signs of endothelium damage and impaired nitric oxide (NO), fat, and energy metabolism. Full article
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