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Cardiogenetics
Volume 13
Issue 1
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Cardiogenetics, Volume 13, Issue 1 (March 2023) – 5 articles

Cover Story (view full-size image): Arrhythmogenic cardiomyopathy (ACM) is an inherited multi-faceted cardiac disease that causes sudden cardiac death. Recent clinical studies have recognized that ventricular arrhythmias were the underlying cause of death in post-COVID-19 patients due to established systemic inflammation associated with viral myocarditis. Currently, the available therapeutic options for treating this disease are either pharmacological or non-pharmacological. The most commonly used option includes an implantable cardioverter defibrillator (ICD) that can prevent further life-threatening actions of fibrillation. However, one of the only other options is heart transplantation. Therefore, there is an imperative need to tackle all these forms of ACM, which might be possible due to genome editing technology. View this paper
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14 pages, 4753 KiB  
Article
Sex Differences in Fatty Acid Metabolism and Blood Pressure Response to Dietary Salt in Humans
by Jeanne A. Ishimwe, Jane F. Ferguson and Annet Kirabo
Cardiogenetics 2023, 13(1), 33-46; https://doi.org/10.3390/cardiogenetics13010005 - 03 Mar 2023
Viewed by 2771
Abstract
Salt sensitivity is a trait in which high dietary sodium (Na+) intake causes an increase in blood pressure (BP). We previously demonstrated that in the gut, elevated dietary Na+ causes dysbiosis. The mechanistic interplay between excess dietary Na+-induced [...] Read more.
Salt sensitivity is a trait in which high dietary sodium (Na+) intake causes an increase in blood pressure (BP). We previously demonstrated that in the gut, elevated dietary Na+ causes dysbiosis. The mechanistic interplay between excess dietary Na+-induced alteration in the gut microbiome and sex differences is less understood. The goal of this study was to identify novel metabolites in sex differences and blood pressure in response to a high dietary Na+ intake. We performed stool and plasma metabolomics analysis and measured the BP of human volunteers with salt intake above or below the American Heart Association recommendations. We also performed RNA sequencing on human monocytes treated with high salt in vitro. The relationship between BP and dietary Na+ intake was different in women and men. Network analysis revealed that fatty acids as top subnetworks differentially changed with salt intake. We found that women with high dietary Na+ intake have high levels of arachidonic acid related metabolism, suggesting a role in sex differences of the blood pressure response to Na+. The exposure of monocytes to high salt in vitro upregulates the transcription of fatty acid receptors and arachidonic acid-related genes. These findings provide potentially novel insights into metabolic changes underlying gut dysbiosis and inflammation in salt sensitivity of BP. Full article
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2 pages, 171 KiB  
Editorial
A Crossroads Junction That Leads to Heart Failure (Arrhythmogenic Cardiomyopathy): Hope for Future Therapeutics
by Kadiam C. Venkata Subbaiah
Cardiogenetics 2023, 13(1), 31-32; https://doi.org/10.3390/cardiogenetics13010004 - 17 Feb 2023
Viewed by 1756
Abstract
Arrhythmogenic cardiomyopathy (ACM) is an inherited multifaceted cardiac disease that causes sudden cardiac death, especially in young adults and athletes [...] Full article
(This article belongs to the Special Issue Genetics of Inherited Arrhythmogenic Syndromes Associated with Sudden Death)
16 pages, 830 KiB  
Article
Lower Circulating Cell-Free Mitochondrial DNA Is Associated with Heart Failure in Type 2 Diabetes Mellitus Patients
by Tetiana A. Berezina, Mykola P. Kopytsya, Olga V. Petyunina, Alexander A. Berezin, Zeljko Obradovic, Lukas Schmidbauer, Michael Lichtenauer and Alexander E. Berezin
Cardiogenetics 2023, 13(1), 15-30; https://doi.org/10.3390/cardiogenetics13010003 - 07 Feb 2023
Cited by 3 | Viewed by 2987
Abstract
Cell-free nuclear (cf-nDNA) and mitochondrial (cf-mDNA) DNA are released from damaged cells in type 2 diabetes mellitus (T2DM) patients, contributing to adverse cardiac remodeling, vascular dysfunction, and inflammation. The purpose of this study was to correlate the presence and type of cf-DNAs with [...] Read more.
Cell-free nuclear (cf-nDNA) and mitochondrial (cf-mDNA) DNA are released from damaged cells in type 2 diabetes mellitus (T2DM) patients, contributing to adverse cardiac remodeling, vascular dysfunction, and inflammation. The purpose of this study was to correlate the presence and type of cf-DNAs with HF in T2DM patients. A total of 612 T2DM patients were prescreened by using a local database, and 240 patients (120 non-HF and 120 HF individuals) were ultimately selected. The collection of medical information, including both echocardiography and Doppler imagery, as well as the assessment of biochemistry parameters and the circulating biomarkers, were performed at baseline. The N-terminal brain natriuretic pro-peptide (NT-proBNP) and cf-nDNA/cf-mtDNA levels were measured via an ELISA kit and real-time quantitative PCR tests, respectively. We found that HF patients possessed significantly higher levels of cf-nDNA (9.9 ± 2.5 μmol/L vs. 5.4 ± 2.7 μmol/L; p = 0.04) and lower cf-mtDNA (15.7 ± 3.3 μmol/L vs. 30.4 ± 4.8 μmol/L; p = 0.001) than those without HF. The multivariate log regression showed that the discriminative potency of cf-nDNA >7.6 μmol/L (OR = 1.07; 95% CI = 1.03–1.12; p = 0.01) was higher that the NT-proBNP (odds ratio [OR] = 1.10; 95% confidence interval [CI] = 1.04–1.19; p = 0.001) for HF. In conclusion, we independently established that elevated levels of cf-nDNA, originating from NT-proBNP, were associated with HF in T2DM patients. Full article
(This article belongs to the Section Biomarkers)
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1 pages, 251 KiB  
Editorial
Acknowledgment to the Reviewers of Cardiogenetics in 2022
by Cardiogenetics Editorial Office
Cardiogenetics 2023, 13(1), 14; https://doi.org/10.3390/cardiogenetics13010002 - 17 Jan 2023
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Abstract
High-quality academic publishing is built on rigorous peer review [...] Full article
13 pages, 2440 KiB  
Article
Anti-Ischemic Effect of Leptin in the Isolated Rat Heart Subjected to Global Ischemia-Reperfusion: Role of Cardiac-Specific miRNAs
by Ekaterina A. Polyakova, Evgeny N. Mikhaylov, Sarkis M. Minasian, Mikhail M. Galagudza and Evgeny V. Shlyakhto
Cardiogenetics 2023, 13(1), 1-13; https://doi.org/10.3390/cardiogenetics13010001 - 04 Jan 2023
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Abstract
Background: Leptin is an obesity-associated adipokine that has been implicated in cardiac protection against ischemia-reperfusion injury (IRI). In this study, concentration-dependent effects of leptin on myocardial IRI were investigated in the isolated rat heart. In addition, we analyzed myocardial miRNAs expression in order [...] Read more.
Background: Leptin is an obesity-associated adipokine that has been implicated in cardiac protection against ischemia-reperfusion injury (IRI). In this study, concentration-dependent effects of leptin on myocardial IRI were investigated in the isolated rat heart. In addition, we analyzed myocardial miRNAs expression in order to investigate their potential involvement in leptin-mediated cardioprotection. Methods: The effect of leptin on IRI was examined in Langendorff-perfused rat hearts preconditioned with two leptin concentrations (1.0 nM and 3.1 nM) for 60 min. The hearts were subjected to 30 min global ischemia and 120 min reperfusion with buffer containing leptin in the respective concentration. Heart function and arrhythmia incidence were analyzed. Infarct size was assessed histochemically. Expression of miRNA-144, -208a, -378, and -499 was analyzed in the ventricular myocardium using RT-PCR. Results: The addition of 1.0 nM leptin to the buffer exerted an infarct-limiting effect, preserved post-ischemic ventricular function, and prevented reperfusion arrhythmia compared to 3.1 nM leptin. Myocardial expression of miRNA-208a was decreased after heart exposure to 1.0 nM leptin and significantly elevated in the hearts perfused with leptin at 3.1 nM. Conclusion: Acute administration of leptin at low dose (1.0 nM) results in cardiac protection against IRI. This effect is associated with reduced myocardial expression of miRNA-208a. Full article
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