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Progress in Prevention and Treatment of Cardiovascular Diseases and Arrhythmias

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Centre of Experimental Medicine, Institute for Heart Research, Slovak Academy of Sciences, 84104 Bratislava, Slovakia
Interests: inflammation; redox disorder; heart diseases; arrhythmia substrate; cardiac connexin-43; Cx-hemichannels; antiarrhythmic mechanisms of tested agents; omega-3 fatty acids; melatonin
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Special Issue Information

Dear Colleagues, 

Although cardiology has progressed dramatically, cardiovascular diseases (CVDs) and malignant arrhythmias remain the most common cause of death worldwide, and much remains to be accomplished. The next major steps should include more vigorous and widespread prevention as well as the application of the recent remarkable advances in genomics. The best way to avoid cardiovascular diseases (CVDs) and cardiac arrhythmias is to prevent their development. One of the most important risk factors of CVDs is an unhealthy lifestyle. Regular medical screening can reveal warning signs or biomarkers like increased blood pressure, blood glucose, lipid profile, C-reactive protein, and body mass index, which indicates a predisposition to diseases before symptoms manifest. Screenings can improve health outcomes via lifestyle modifications, such as diet, exercise, cold acclimation, or treatment interventions. There is a need to mitigate climate change due to the greenhouse gas emission-associated cardiovascular risk, particularly in vulnerable populations. Recent advancements highlight the potential of naturally derived bio-products with epigenetic properties which offer protection against CVDs and cardiac arrhythmias. To reach the optimal level of protection, a multi-targeted approach directed towards more than one intracellular signaling pathway or cell type is required. One of the most studied targets are mitochondria because of their key involvement in reactive oxygen species (ROS) production facilitating chronic low-grade inflammation that predispose to CVDs and arrhythmias. On the other hand, hydrogen medicine is one of the most promising novel strategies for the prevention and/or treatment of these adverse conditions via molecular hydrogen. "There is still time to share your science’’.

Dr. Narcis Tribulova
Guest Editor

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Keywords

  • translational research
  • novel animal models
  • novel treatment targets
  • pleiotropic drugs
  • harnessing of molecular H

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Published Papers (2 papers)

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Research

12 pages, 919 KB  
Article
An Explorative Approach to Examining the Role of Ischemia and Inflammation on the Function of Autoantibodies Against G Protein–Coupled Receptors and Their Corresponding Agonists
by Gerd Wallukat, Petra Lakatos, Kira Steinhorst, Merle Flecks and Bettina Hohberger
Int. J. Mol. Sci. 2026, 27(6), 2797; https://doi.org/10.3390/ijms27062797 - 19 Mar 2026
Viewed by 382
Abstract
Autoantibodies (AAbs) play an important role in the development of autoimmune diseases. While many AAbs induce apoptosis of target cells, a distinct subgroup, termed functional autoantibodies (fAAbs) against G protein–coupled receptors (GPCRs), can modulate physiological receptor signaling without inducing cell death. The functional [...] Read more.
Autoantibodies (AAbs) play an important role in the development of autoimmune diseases. While many AAbs induce apoptosis of target cells, a distinct subgroup, termed functional autoantibodies (fAAbs) against G protein–coupled receptors (GPCRs), can modulate physiological receptor signaling without inducing cell death. The functional activity of GPCR-fAAbs may be influenced by various cofactors, including inflammation (e.g., inflammatory cytokine, ciliary neurotrophic factor (CNTF)) and ischemia. As ischemia triggers a substantial release of arachidonic acid (AA) from membrane phospholipids, the present study aimed to examine exploratively the influence of AA, eicosapentaenoic acid (EPA), and CNTF on the responses of spontaneously beating neonatal rat cardiomyocytes to GPCR agonists and GPCR-fAAbs. AA and EPA differentially influenced responses in cardiomyocytes induced by GPCR-fAAbs: AA altered the functional responses associated with adrenergic β2-fAAb, adrenergic α1-fAAb, angiotensin II (AT1)-fAAb, endothelin A (ETA)-fAAb and angiotensin 1–7 MAS-fAAbs. However, muscarinergic M2-fAAb responses remained largely unaffected. In contrast, EPA attenuated the responses to β2-fAAb, α1-fAAb, AT1-fAAb, and ETA-fAAb, while MAS-fAAb and M2-fAAb responses were not markedly altered. CNTF acted as a time-dependent modulator of cardiomyocyte chronotropic responses and influenced the magnitude of GPCR-mediated signaling on a cardiomyocyte bioassay. Together, these findings might suggest that lipid mediators such as AA and EPA or CNTF may modulate functional responses of cardiomyocytes associated with GPCR-fAAbs. Full article
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23 pages, 3763 KB  
Article
Effect of Sacubitril/Valsartan, Ivabradine, and Captopril on Anxiety-like Behavior in Spontaneously Hypertensive Rats
by Maria Szighardtova, Silvia Aziriova, Peter Stanko, Kristina Repova, Tomas Baka, Kristina Krajcirovicova, Stefan Zorad, Michaela Adamcova, Peter Sabaka, Veronika Borbélyová and Fedor Simko
Int. J. Mol. Sci. 2025, 26(22), 10905; https://doi.org/10.3390/ijms262210905 - 10 Nov 2025
Cited by 2 | Viewed by 1239
Abstract
Cardiovascular disorders and the medications used to treat them can affect physiological patterns of behavior. The aim of the present study was to determine whether the dual inhibition of neprilysin and angiotensin II—sacubitril/valsartan (ARNI) can modify anxiety-like behavior in male spontaneously hypertensive rats [...] Read more.
Cardiovascular disorders and the medications used to treat them can affect physiological patterns of behavior. The aim of the present study was to determine whether the dual inhibition of neprilysin and angiotensin II—sacubitril/valsartan (ARNI) can modify anxiety-like behavior in male spontaneously hypertensive rats (SHR). We compared ARNI with two other drugs in the portfolio of heart failure treatment, captopril and ivabradine. Six groups (n = 13) of 12-week-old rats were treated for six weeks: control (Wistar rats), control + ARNI, SHR, SHR + ARNI, SHR + captopril, and SHR + ivabradine. The elevated plus maze test, the open field test, and the light–dark box test were used to determine anxiety-like behavior. SHRs exhibited higher systolic blood pressure (SBP), heart rate (HR), left ventricular weight (LVW), and hydroxyproline concentration (LVHP) but displayed a reduced level of anxiety-like behavior in comparison to controls. ARNI reduced SBP, HR, and LVW but had no significant effect on the level of anxiety in SHR, and similar results were achieved by captopril and ivabradine. Additionally, correlation analysis indicated that anxiety-like behavior in Wistar rats or SHR, either with or without cardiovascular therapy, was independent of SBP, HR, LVW, or LVHP. The level of anxiety-like behavior can, therefore, be considered part of the inherent neurobehavioral traits unrelated to fundamental hemodynamic or structural cardiovascular parameters. Full article
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