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Molecular Biology of Atrial Myocardium
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Molecular Biology of Atrial Myocardium

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cells of the Cardiovascular System".

Deadline for manuscript submissions: closed (30 June 2023) | Viewed by 16709

Special Issue Editor

Prof. Dr. Andreas Goette

E-Mail Website
Guest Editor
1. Department of Cardiology and Intensive Care Medicine, St. Vincenz Hospital, 33098 Paderborn, Germany
2. MAESTRIA Consortium/AFNET, 48149 Münster, Germany
Interests: arrhythmia; atrial fibrillation; molecular biology; electrophysiology; thrombogenesis

Special Issue Information

Dear Colleagues,

The term atrial cardiomyopathy was first introduced in 2016. Many studies have linked the presence of atrial tissue changes to the development of atrial fibrillation (AF) and stroke. Several molecular changes within the atrial myocardium are activated by concomitant diseases or behaviors such as hypertension, heart failure, valve diseases, diabetes mellitus, and smoking prior to the development of atrial arrhythmia. Therefore, this Special Issue will summarize changes in molecular biology of the atria, which are induced by concomitant diseases. In particular, the effects of diabetes mellitus, hypertension, adipocytes, oxidative stress, smoking, alcohol, and inflammasome will be explained and highlighted in detail. Thus, this Special Issue will provide a unique and comprehensive summary of the molecular biology of atrial myocardium.

Content:

  • Atrial myocardium in diabetes mellitus
  • Atrial myocardium in arterial hypertension
  • Atrial myocardium and epicardial fat tissue
  • Atrial myocardium and oxidative stress
  • Atrial myocardium and cigarette smoking
  • Atrial myocardium and alcohol consumption
  • Atrial myocardium and the inflammasome
  • Atrial myocardium and systemic biomarkers
  • Atrial myocardium and thrombogenesis

Prof. Dr. Andreas Goette
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. Cells is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). 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.

Published Papers (7 papers)

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Research

Jump to: Review

23 pages, 3189 KiB  
Article
Coagulation Factor Xa Has No Effects on the Expression of PAR1, PAR2, and PAR4 and No Proinflammatory Effects on HL-1 Cells
by Lukas Ruf, Alicja Bukowska, Andreas Gardemann and Andreas Goette
Cells 2023, 12(24), 2849; https://doi.org/10.3390/cells12242849 - 15 Dec 2023
Viewed by 1016
Abstract
Atrial fibrillation (AF), characterised by irregular high-frequency contractions of the atria of the heart, is of increasing clinical importance. The reasons are the increasing prevalence and thromboembolic complications caused by AF. So-called atrial remodelling is characterised, among other things, by atrial dilatation and [...] Read more.
Atrial fibrillation (AF), characterised by irregular high-frequency contractions of the atria of the heart, is of increasing clinical importance. The reasons are the increasing prevalence and thromboembolic complications caused by AF. So-called atrial remodelling is characterised, among other things, by atrial dilatation and fibrotic remodelling. As a result, AF is self-sustaining and forms a procoagulant state. But hypercoagulation not only appears to be the consequence of AF. Coagulation factors can exert influence on cells via protease-activated receptors (PAR) and thereby the procoagulation state could contribute to the development and maintenance of AF. In this work, the influence of FXa on Heart Like-1 (HL-1) cells, which are murine adult atrial cardiomyocytes (immortalized), was investigated. PAR1, PAR2, and PAR4 expression was detected. After incubations with FXa (5–50 nM; 4–24 h) or PAR1- and PAR2-agonists (20 µM; 4–24 h), no changes occurred in PAR expression or in the inflammatory signalling cascade. There were no time- or concentration-dependent changes in the phosphorylation of the MAP kinases ERK1/2 or the p65 subunit of NF-κB. In addition, there was no change in the mRNA expression of the cell adhesion molecules (ICAM-1, VCAM-1, fibronectin). Thus, FXa has no direct PAR-dependent effects on HL-1 cells. Future studies should investigate the influence of FXa on human cardiomyocytes or on other cardiac cell types like fibroblasts. Full article
(This article belongs to the Special Issue Molecular Biology of Atrial Myocardium)
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17 pages, 1472 KiB  
Article
Cytotoxic CD8+ T Cells Are Involved in the Thrombo-Inflammatory Response during First-Diagnosed Atrial Fibrillation
by Julian Friebel, Marco Witkowski, Max Wegner, Leon Blöbaum, Stella Lammel, Philipp-Alexander Schencke, Kai Jakobs, Marianna Puccini, Daniela Reißner, Daniel Steffens, Verena Moos, Heinz-Peter Schutheiss, Ulf Landmesser and Ursula Rauch
Cells 2023, 12(1), 141; https://doi.org/10.3390/cells12010141 - 29 Dec 2022
Cited by 5 | Viewed by 2074
Abstract
Background: Atrial myopathy and atrial fibrillation (AF) accompany thrombo-inflammation. This facilitates disease progression and promotes major adverse cardiovascular events (MACEs). Thrombin receptor (protease-activated receptor 1, PAR1) signalling is central in mediating thrombo-inflammation. We hypothesised that PAR1 signalling links coagulation and inflammation through cytotoxic [...] Read more.
Background: Atrial myopathy and atrial fibrillation (AF) accompany thrombo-inflammation. This facilitates disease progression and promotes major adverse cardiovascular events (MACEs). Thrombin receptor (protease-activated receptor 1, PAR1) signalling is central in mediating thrombo-inflammation. We hypothesised that PAR1 signalling links coagulation and inflammation through cytotoxic CD8+ T lymphocytes in patients presenting with first-diagnosed AF (FDAF). Methods: A total of 210 patients were studied. We included data and blood samples from patients presenting with FDAF (n = 160), cardiac tissue from patients with paroxysmal AF (n = 32) and 20 controls. Results: During early AF, a pro-inflammatory and cytotoxic subset of T lymphocytes (CD8+) circulated more frequently when compared to patients with chronic cardiovascular disease but without AF, accompanied by elevated plasma levels of CD8+ effector molecules, which corresponded to biomarkers of adverse cardiac remodelling and atrial dysfunction. Activation of tissue factor (TF) and PAR1 was associated with pro-inflammatory and cytotoxic effector functions. PAR1-related CD8+ cell activation was more frequent in FDAF patients that experienced a MACE. Conclusions: In patients with FDAF, the TF-factor Xa-factor IIa-axis contributes to thrombo-inflammation via PAR1 in CD8+ T cells. Intervening in this cascade might be a promising synergistic approach to reducing disease progression and the vascular complications of AF. Full article
(This article belongs to the Special Issue Molecular Biology of Atrial Myocardium)
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15 pages, 2491 KiB  
Article
Peculiarities of the Acetylcholine Action on the Contractile Function of Cardiomyocytes from the Left and Right Atria in Rats
by Xenia Butova, Tatiana Myachina, Raisa Simonova, Anastasia Kochurova, Yakov Bozhko, Michael Arkhipov, Olga Solovyova, Galina Kopylova, Daniil Shchepkin and Anastasia Khokhlova
Cells 2022, 11(23), 3809; https://doi.org/10.3390/cells11233809 - 28 Nov 2022
Cited by 1 | Viewed by 1479
Abstract
Acetylcholine (ACh) is the neurotransmitter of the parasympathetic nervous system that modulates cardiac function, and its high concentrations may induce atrial fibrillation. We compared the ACh action on the mechanical function of single cardiomyocytes from the left atria (LA) and the right atria [...] Read more.
Acetylcholine (ACh) is the neurotransmitter of the parasympathetic nervous system that modulates cardiac function, and its high concentrations may induce atrial fibrillation. We compared the ACh action on the mechanical function of single cardiomyocytes from the left atria (LA) and the right atria (RA). We exposed single rat LA and RA cardiomyocytes to 1, 10, and 100 µM ACh for 10–15 min and measured the parameters of sarcomere shortening–relengthening and cytosolic calcium ([Ca2+]i) transients during cell contractions. We also studied the effects of ACh on cardiac myosin function using an in vitro motility assay and analyzed the phosphorylation level of sarcomeric proteins. In LA cardiomyocytes, ACh decreased the time to peak sarcomere shortening, time to 50% relengthening, and time to peak [Ca2+]i transients. In RA cardiomyocytes, ACh affected the time of shortening and relengthening only at 10 µM. In the in vitro motility assay, ACh reduced to a greater extent the sliding velocity of F-actin over myosin from LA cardiomyocytes, which was accompanied by a more pronounced decrease in phosphorylation of the myosin regulatory light chain (RLC) in LA cardiomyocytes than in RA cardiomyocytes. Our findings indicate that ACh plays an important role in modulating the contractile function of LA and RA, provoking more pronounced changes in the time course of sarcomere shortening–relengthening and the kinetics of actin–myosin interaction in LA cardiomyocytes. Full article
(This article belongs to the Special Issue Molecular Biology of Atrial Myocardium)
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Review

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26 pages, 2475 KiB  
Review
Atrial Cardiomyopathy in Valvular Heart Disease: From Molecular Biology to Clinical Perspectives
by Andrea Ágnes Molnár, Attila Sánta, Dorottya Tímea Pásztor and Béla Merkely
Cells 2023, 12(13), 1796; https://doi.org/10.3390/cells12131796 - 6 Jul 2023
Cited by 5 | Viewed by 3328
Abstract
This review discusses the evolving topic of atrial cardiomyopathy concerning valvular heart disease. The pathogenesis of atrial cardiomyopathy involves multiple factors, such as valvular disease leading to atrial structural and functional remodeling due to pressure and volume overload. Atrial enlargement and dysfunction can [...] Read more.
This review discusses the evolving topic of atrial cardiomyopathy concerning valvular heart disease. The pathogenesis of atrial cardiomyopathy involves multiple factors, such as valvular disease leading to atrial structural and functional remodeling due to pressure and volume overload. Atrial enlargement and dysfunction can trigger atrial tachyarrhythmia. The complex interaction between valvular disease and atrial cardiomyopathy creates a vicious cycle of aggravating atrial enlargement, dysfunction, and valvular disease severity. Furthermore, atrial remodeling and arrhythmia can predispose to atrial thrombus formation and stroke. The underlying pathomechanism of atrial myopathy involves molecular, cellular, and subcellular alterations resulting in chronic inflammation, atrial fibrosis, and electrophysiological changes. Atrial dysfunction has emerged as an essential determinant of outcomes in valvular disease and heart failure. Despite its predictive value, the detection of atrial fibrosis and dysfunction is challenging and is not included in the clinical routine. Transthoracic echocardiography and cardiac magnetic resonance imaging are the main diagnostic tools for atrial cardiomyopathy. Recently published data have revealed that both left atrial volumes and functional parameters are independent predictors of cardiovascular events in valvular disease. The integration of atrial function assessment in clinical practice might help in early cardiovascular risk estimation, promoting early therapeutic intervention in valvular disease. Full article
(This article belongs to the Special Issue Molecular Biology of Atrial Myocardium)
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26 pages, 940 KiB  
Review
Left Atrial Myocardium in Arterial Hypertension
by Jens Kockskämper and Florentina Pluteanu
Cells 2022, 11(19), 3157; https://doi.org/10.3390/cells11193157 - 8 Oct 2022
Cited by 11 | Viewed by 3169
Abstract
Arterial hypertension affects ≈ 1 billion people worldwide. It is associated with increased morbidity and mortality and responsible for millions of deaths each year. Hypertension mediates damage of target organs including the heart. In addition to eliciting left ventricular hypertrophy, dysfunction and heart [...] Read more.
Arterial hypertension affects ≈ 1 billion people worldwide. It is associated with increased morbidity and mortality and responsible for millions of deaths each year. Hypertension mediates damage of target organs including the heart. In addition to eliciting left ventricular hypertrophy, dysfunction and heart failure, hypertension also causes left atrial remodeling that may culminate in atrial contractile dysfunction and atrial fibrillation. Here, we will summarize data on the various aspects of left atrial remodeling in (essential) hypertension gathered from studies on patients with hypertension and from spontaneously hypertensive rats, an animal model that closely mimics cardiac remodeling in human hypertension. Analyzing the timeline of remodeling processes, i.e., distinguishing between alterations occurring in prehypertension, in early hypertension and during advanced hypertensive heart disease, we will derive the potential mechanisms underlying left atrial remodeling in (essential) hypertension. Finally, we will discuss the consequences of these remodeling processes for atrial and ventricular function. The data imply that left atrial remodeling is multifactorial, starts early in hypertension and is an important contributor to the progression of hypertensive heart disease, including the development of atrial fibrillation and heart failure. Full article
(This article belongs to the Special Issue Molecular Biology of Atrial Myocardium)
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15 pages, 2006 KiB  
Review
The Complex Relation between Atrial Cardiomyopathy and Thrombogenesis
by Elisa D’Alessandro, Joris Winters, Frans A. van Nieuwenhoven, Ulrich Schotten and Sander Verheule
Cells 2022, 11(19), 2963; https://doi.org/10.3390/cells11192963 - 22 Sep 2022
Cited by 3 | Viewed by 1924
Abstract
Heart disease, as well as systemic metabolic alterations, can leave a ‘fingerprint’ of structural and functional changes in the atrial myocardium, leading to the onset of atrial cardiomyopathy. As demonstrated in various animal models, some of these changes, such as fibrosis, cardiomyocyte hypertrophy [...] Read more.
Heart disease, as well as systemic metabolic alterations, can leave a ‘fingerprint’ of structural and functional changes in the atrial myocardium, leading to the onset of atrial cardiomyopathy. As demonstrated in various animal models, some of these changes, such as fibrosis, cardiomyocyte hypertrophy and fatty infiltration, can increase vulnerability to atrial fibrillation (AF), the most relevant manifestation of atrial cardiomyopathy in clinical practice. Atrial cardiomyopathy accompanying AF is associated with thromboembolic events, such as stroke. The interaction between AF and stroke appears to be far more complicated than initially believed. AF and stroke share many risk factors whose underlying pathological processes can reinforce the development and progression of both cardiovascular conditions. In this review, we summarize the main mechanisms by which atrial cardiomyopathy, preceding AF, supports thrombogenic events within the atrial cavity and myocardial interstitial space. Moreover, we report the pleiotropic effects of activated coagulation factors on atrial remodeling, which may aggravate atrial cardiomyopathy. Finally, we address the complex association between AF and stroke, which can be explained by a multidirectional causal relation between atrial cardiomyopathy and hypercoagulability. Full article
(This article belongs to the Special Issue Molecular Biology of Atrial Myocardium)
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29 pages, 2805 KiB  
Review
Harmful Impact of Tobacco Smoking and Alcohol Consumption on the Atrial Myocardium
by Amelie H. Ohlrogge, Lars Frost and Renate B. Schnabel
Cells 2022, 11(16), 2576; https://doi.org/10.3390/cells11162576 - 18 Aug 2022
Cited by 7 | Viewed by 3025
Abstract
Tobacco smoking and alcohol consumption are widespread exposures that are legal and socially accepted in many societies. Both have been widely recognized as important risk factors for diseases in all vital organ systems including cardiovascular diseases, and with clinical manifestations that are associated [...] Read more.
Tobacco smoking and alcohol consumption are widespread exposures that are legal and socially accepted in many societies. Both have been widely recognized as important risk factors for diseases in all vital organ systems including cardiovascular diseases, and with clinical manifestations that are associated with atrial dysfunction, so-called atrial cardiomyopathy, especially atrial fibrillation and stroke. The pathogenesis of atrial cardiomyopathy, atrial fibrillation, and stroke in context with smoking and alcohol consumption is complex and multifactorial, involving pathophysiological mechanisms, environmental, and societal aspects. This narrative review summarizes the current literature regarding alterations in the atrial myocardium that is associated with smoking and alcohol. Full article
(This article belongs to the Special Issue Molecular Biology of Atrial Myocardium)
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