Molecular and Cellular Mechanisms of Diseases: Heart Disease

Topic Information

Dear Colleagues,

Heart failure is still a leading cause of mortality worldwide. Cardiomyocytes contribute to heart failure by losing the ability to generate sufficient force to pump blood into circulation. To improve the current treatment options in cardiology, it is important to have a better understanding of the biological behavior of cardiomyocytes. The function of these cells cannot be completely understood independently of the interaction with surrounding cells, i.e., cardiac fibroblasts and vascular cells. Nevertheless, cardiomyocytes are the cells that must generate heart work. They can modify parts of their electromechanical coupling machinery, electrometabolic coupling, or increase in size via hypertrophy. However, hypertrophy can be either adaptive or maladaptive and the transition from the one into the other type of hypertrophy is not clearly understood. Processes dealing with metabolism, electromechanical coupling, and electrophysiological aspects are among the processes that need to be addressed and understood in their molecular fine regulation in order to improve treatment regimes. This Topic aims to summarize the current understanding of the process of developing heart failure with a focus on the force-generating cell, the cardiomyocyte.

Prof. Dr. Klaus-Dieter Schlüter
Prof. Dr. Pasi Tavi
Prof. Dr. Ebru Arioglu-Inan
Topic Editors

Keywords

Participating Journals

Journal Name	Impact Factor	CiteScore	Launched Year	First Decision (median)	APC
Biomolecules biomolecules	4.8	9.4	2011	16.3 Days	CHF 2700
Cells cells	5.1	9.9	2012	17.5 Days	CHF 2700
Diseases diseases	2.9	0.8	2013	18.9 Days	CHF 1800
International Journal of Molecular Sciences ijms	4.9	8.1	2000	18.1 Days	CHF 2900
Journal of Molecular Pathology jmp	-	-	2020	25.4 Days	CHF 1000
Organoids organoids	-	-	2022	15.0 days *	CHF 1000
Journal of Cardiovascular Development and Disease jcdd	2.4	2.6	2014	22.9 Days	CHF 2700

* Median value for all MDPI journals in the first half of 2024.

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Published Papers (12 papers)

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31 pages, 1810 KiB  

Open AccessReview

Mitochondrial Kinase Signaling for Cardioprotection

by Kerstin Boengler, Chantal Eickelmann and Petra Kleinbongard

Int. J. Mol. Sci. 2024, 25(8), 4491; https://doi.org/10.3390/ijms25084491 - 19 Apr 2024

Viewed by 1223

Abstract

Myocardial ischemia/reperfusion injury is reduced by cardioprotective adaptations such as local or remote ischemic conditioning. The cardioprotective stimuli activate signaling cascades, which converge on mitochondria and maintain the function of the organelles, which is critical for cell survival. The signaling cascades include not [...] Read more.

Myocardial ischemia/reperfusion injury is reduced by cardioprotective adaptations such as local or remote ischemic conditioning. The cardioprotective stimuli activate signaling cascades, which converge on mitochondria and maintain the function of the organelles, which is critical for cell survival. The signaling cascades include not only extracellular molecules that activate sarcolemmal receptor-dependent or -independent protein kinases that signal at the plasma membrane or in the cytosol, but also involve kinases, which are located to or within mitochondria, phosphorylate mitochondrial target proteins, and thereby modify, e.g., respiration, the generation of reactive oxygen species, calcium handling, mitochondrial dynamics, mitophagy, or apoptosis. In the present review, we give a personal and opinionated overview of selected protein kinases, localized to/within myocardial mitochondria, and summarize the available data on their role in myocardial ischemia/reperfusion injury and protection from it. We highlight the regulation of mitochondrial function by these mitochondrial protein kinases. Full article

(This article belongs to the Topic Molecular and Cellular Mechanisms of Diseases: Heart Disease)

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20 pages, 7399 KiB  

Open AccessArticle

Unraveling Desmin’s Head Domain Structure and Function

by Dimitrios Vlachakis, Konstantinos Tsilafakis, Ioanna Kostavasili, Sophia Kossida and Manolis Mavroidis

Cells 2024, 13(7), 603; https://doi.org/10.3390/cells13070603 - 29 Mar 2024

Cited by 1 | Viewed by 1091

Abstract

Understanding the structure and function of intermediate filaments (IFs) is necessary in order to explain why more than 70 related IF genes have evolved in vertebrates while maintaining such dramatically tissue-specific expression. Desmin is a member of the large multigene family of IF [...] Read more.

Understanding the structure and function of intermediate filaments (IFs) is necessary in order to explain why more than 70 related IF genes have evolved in vertebrates while maintaining such dramatically tissue-specific expression. Desmin is a member of the large multigene family of IF proteins and is specifically expressed in myocytes. In an effort to elucidate its muscle-specific behavior, we have used a yeast two-hybrid system in order to identify desmin’s head binding partners. We described a mitochondrial and a lysosomal protein, NADH ubiquinone oxidoreductase core subunit S2 (NDUFS2), and saposin D, respectively, as direct desmin binding partners. In silico analysis indicated that both interactions at the atomic level occur in a very similar way, by the formation of a three-helix bundle with hydrophobic interactions in the interdomain space and hydrogen bonds at R16 and S32 of the desmin head domain. The interactions, confirmed also by GST pull-down assays, indicating the necessity of the desmin head domain and, furthermore, point out its role in function of mitochondria and lysosomes, organelles which are disrupted in myopathies due to desmin head domain mutations. Full article

(This article belongs to the Topic Molecular and Cellular Mechanisms of Diseases: Heart Disease)

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23 pages, 9776 KiB  

Open AccessArticle

Functional and Multi-Omics Effects of an Optimized CRISPR-Mediated FURIN Depletion in U937 Monocytes

by Ruiming Chua, Lijin Wang, Roshni Singaraja and Sujoy Ghosh

Cells 2024, 13(7), 588; https://doi.org/10.3390/cells13070588 - 28 Mar 2024

Viewed by 1401

Abstract

The pro-protein convertase FURIN (PCSK3) is implicated in a wide range of normal and pathological biological processes such as infectious diseases, cancer and cardiovascular diseases. Previously, we performed a systemic inhibition of FURIN in a mouse model of atherosclerosis and demonstrated significant plaque [...] Read more.

The pro-protein convertase FURIN (PCSK3) is implicated in a wide range of normal and pathological biological processes such as infectious diseases, cancer and cardiovascular diseases. Previously, we performed a systemic inhibition of FURIN in a mouse model of atherosclerosis and demonstrated significant plaque reduction and alterations in macrophage function. To understand the cellular mechanisms affected by FURIN inhibition in myeloid cells, we optimized a CRISPR-mediated gene deletion protocol for successfully deriving hemizygous (HZ) and nullizygous (NZ) FURIN knockout clones in U937 monocytic cells using lipotransfection-based procedures and a dual guide RNA delivery strategy. We observed differences in monocyte and macrophage functions involving phagocytosis, lipid accumulation, cell migration, inflammatory gene expression, cytokine release patterns, secreted proteomics (cytokines) and whole-genome transcriptomics between wild-type, HZ and NZ FURIN clones. These studies provide a mechanistic basis on the possible roles of myeloid cell FURIN in cardiovascular disorders. Full article

(This article belongs to the Topic Molecular and Cellular Mechanisms of Diseases: Heart Disease)

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18 pages, 4723 KiB  

Open AccessSystematic Review

Istaroxime for Patients with Acute Heart Failure: A Systematic Review and Meta-Analysis of Randomized Controlled Trials

by Mohamed Abuelazm, Shafaqat Ali, Majd M. AlBarakat, Abdelrahman Mahmoud, Mohammad Tanashat, Husam Abu Suilik, Basel Abdelazeem and James Robert Brašić

Diseases 2023, 11(4), 183; https://doi.org/10.3390/diseases11040183 - 17 Dec 2023

Cited by 2 | Viewed by 2606

Abstract

Istaroxime, an intravenous inotropic agent with a dual mechanism—increasing both cardiomyocyte contractility and relaxation—is a novel treatment for acute heart failure (AHF), the leading cause of morbidity and mortality in heart failure. We conducted a systematic review and meta-analysis that synthesized randomized controlled [...] Read more.

Istaroxime, an intravenous inotropic agent with a dual mechanism—increasing both cardiomyocyte contractility and relaxation—is a novel treatment for acute heart failure (AHF), the leading cause of morbidity and mortality in heart failure. We conducted a systematic review and meta-analysis that synthesized randomized controlled trials (RCTs), which were retrieved by systematically searching PubMed, Web of Science, SCOPUS, and Cochrane until 24 April 2023. We used a fixed-effect or random-effect model—according to heterogeneity—to pool dichotomous data using the risk ratio (RR) and continuous data using the mean difference (MD), with a 95% confidence interval (CI). We included three RCTs with a total of 300 patients. Istaroxime was significantly associated with an increased left ventricular ejection fraction (mL) (MD: 1.06, 95% CI: 0.29, 1.82; p = 0.007), stroke volume index (MD: 3.04, 95% CI: 2.41, 3.67; p = 0.00001), and cardiac index (L/min/m²) (MD: 0.18, 95% CI: 0.11, 025; p = 0.00001). Also, istaroxime was significantly associated with a decreased E/A ratio (MD: −0.39, 95% CI: −0.58, −0.19; p = 0.0001) and pulmonary artery systolic pressure (mmHg) (MD: 2.30, 95% CI: 3.20, 1.40; p = 0.00001). Istaroxime was significantly associated with increased systolic blood pressure (mmHg) (MD: 5.32, 95% CI: 2.28, 8.37; p = 0.0006) and decreased heart rate (bpm) (MD: −3.05, 95% CI: −5.27, −0.82; p = 0.007). Since istaroxime improved hemodynamic and echocardiographic parameters, it constitutes a promising strategy for AHF management. However, the current literature is limited to a small number of RCTs, warranting further large-scale phase III trials before clinical endorsement. Full article

(This article belongs to the Topic Molecular and Cellular Mechanisms of Diseases: Heart Disease)

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15 pages, 1490 KiB  

Open AccessArticle

Circulating and Cardiac Tissue miRNAs in Children with Dilated Cardiomyopathy

by Frehiwet T. Hailu, Anis Karimpour-Fard, Bonnie Neltner, Brian L. Stauffer, Steven Lipshultz, Shelley D. Miyamoto and Carmen C. Sucharov

J. Cardiovasc. Dev. Dis. 2023, 10(9), 391; https://doi.org/10.3390/jcdd10090391 - 11 Sep 2023

Viewed by 1441

Abstract

microRNAs (miRs) are small non-coding single-stranded RNAs that regulate gene expression. We previously evaluated expression of miRs in the cardiac tissue of children with dilated cardiomyopathy (DCM) using miRNA-seq. However, a comparative analysis of serum and cardiac miRs has not been performed in [...] Read more.

microRNAs (miRs) are small non-coding single-stranded RNAs that regulate gene expression. We previously evaluated expression of miRs in the cardiac tissue of children with dilated cardiomyopathy (DCM) using miRNA-seq. However, a comparative analysis of serum and cardiac miRs has not been performed in this population. The current study aimed to evaluate miR levels in the serum of pediatric DCM patients compared to healthy non-failing (NF) donor controls and investigate the association between miR levels in tissue and sera from the same pediatric DCM patients. Defining the relationship between serum and tissue miRs may allow the use of circulating miRs as surrogate markers of cardiac miRs. miR levels were investigated through miR-array in sera [n = 10 NF, n = 12 DCM] and miR-seq in tissue (n = 10 NF, n = 12 DCM). Pathway analysis was investigated using the miR enrichment analysis and annotation tool (miEAA) for the five miRs commonly dysregulated in the sera and tissue of pediatric DCM patients. Functional analysis of miRs commonly dysregulated in the sera and tissue of pediatric DCM patients suggests altered pathways related to cell growth, differentiation and proliferation, inflammation, mitochondrial function, and metabolism. These findings suggest that circulating miRs could reflect altered levels of cardiac tissue miRs. Full article

(This article belongs to the Topic Molecular and Cellular Mechanisms of Diseases: Heart Disease)

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7 pages, 246 KiB  

Open AccessStudy Protocol

Relationship between Burnout, Cardiovascular Risk Factors, and Inflammatory Markers: A Protocol for Scoping Review

by Oladimeji Adebayo, Misheck J. Nkhata, Kehinde K. Kanmodi, Taiwo Alatishe, Eyinade Egbedina, Temitope Ojo, Samson Ojedokun, John Oladapo, Abiodun Moshood Adeoye and Lawrence A. Nnyanzi

J. Mol. Pathol. 2023, 4(3), 189-195; https://doi.org/10.3390/jmp4030017 - 4 Aug 2023

Viewed by 2058

Abstract

Background: Burnout is increasingly being recognized as a contributory factor to the erosion of a positive psychological state. Studies have examined the relationship between burnout and various inflammatory markers such as IL-1, IL-6, and TNF-alpha. Burnout is also associated with increased systemic inflammation [...] Read more.

Background: Burnout is increasingly being recognized as a contributory factor to the erosion of a positive psychological state. Studies have examined the relationship between burnout and various inflammatory markers such as IL-1, IL-6, and TNF-alpha. Burnout is also associated with increased systemic inflammation along a continuum of symptom severity. This protocol is for a scoping review looking at the link between burnout, inflammatory markers, and cardiovascular risks or diseases. Methods: This study will be based on the preferred reporting items for systematic reviews and meta-analyses guidelines/checklists and the report of the review will be based on the same guideline. The study seeks to address the following principal questions. (i) What are the relevant inflammatory biomarkers that mediate cardiovascular risk factors in burnout? (ii) How do inflammatory biomarkers mediate cardiovascular risk factors in burnout? The outputs obtained from the literature search will be deduplicated using the Rayyan software. Results: We would create table summaries of findings to inform a narrative synthesis of the evidence from the papers included. Conclusion: The review article would help to concisely synthesize the available evidence on the relationship between burnout, inflammatory markers, and cardiovascular diseases. Full article

(This article belongs to the Topic Molecular and Cellular Mechanisms of Diseases: Heart Disease)

21 pages, 4207 KiB  

Open AccessSystematic Review

Contact Force-Guided versus Contact Force-Blinded Cavo-Tricuspid Isthmus Ablation for Atrial Flutter: A Systematic Review and Meta-Analysis

by Mohamed Abuelazm, Islam Mohamed, Amith Reddy Seri, Omar Almaadawy, Basel Abdelazeem and James Robert Brašić

Diseases 2023, 11(3), 98; https://doi.org/10.3390/diseases11030098 - 20 Jul 2023

Viewed by 1778

Abstract

Contact force (CF) is a novel approach developed to increase the safety and efficacy of catheter ablation. However, the value of CF-sensing technology for atrial flutter (AFL) cavo-tricuspid isthmus ablation (CTIA) is inconclusive. To generate a comprehensive assessment of optimal extant data on [...] Read more.

Contact force (CF) is a novel approach developed to increase the safety and efficacy of catheter ablation. However, the value of CF-sensing technology for atrial flutter (AFL) cavo-tricuspid isthmus ablation (CTIA) is inconclusive. To generate a comprehensive assessment of optimal extant data on CF for AFL, we synthesized randomized controlled trials (RCTs) and observational studies from Web of Science, SCOPUS, EMBASE, PubMed, and Cochrane until 29 November 2022, using the odds ratio (OR) for dichotomous outcomes and mean difference (MD) for continuous outcomes with a corresponding 95% confidence interval (CI). Two RCTs and three observational studies with a total of 376 patients were included in our analysis. CF-guided ablation was associated with (A) a higher rate of AFL recurrence (OR: 2.26 with 95% CI [1.05, 4.87]) and total CF (MD: 2.71 with 95% CI [1.28, 4.13]); (B) no effect on total procedure duration (MD: −2.88 with 95% CI [−7.48, 1.72]), fluoroscopy duration (MD: −0.96 with 95% CI [−2.24, 0.31]), and bidirectional isthmus block (BDIB) (OR: 1.50 with 95% CI [0.72, 3.11]); and (C) decreased radiofrequency (RF) duration (MD: −1.40 with 95% CI [−2.39, −0.41]). We conclude that although CF-guided CTIA was associated with increased AFL recurrence and total CF and reduced RF duration, it did not affect total procedure duration, fluoroscopy duration, or BDIB. Thus, CF-guided CTIA may not be the optimal intervention for AFL. These findings indicate the need for (A) providers to balance the benefits and risks of CF when utilizing precision medicine to develop treatment plans for individuals with AFL and (B) clinical trials investigating CF-guided catheter ablation for AFL to provide definitive evidence of optimal CF-sensing technology. Full article

(This article belongs to the Topic Molecular and Cellular Mechanisms of Diseases: Heart Disease)

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13 pages, 643 KiB  

Open AccessReview

Emerging Role and Mechanism of the FTO Gene in Cardiovascular Diseases

by Zi-Yang Xu, Xia Jing and Xing-Dong Xiong

Biomolecules 2023, 13(5), 850; https://doi.org/10.3390/biom13050850 - 17 May 2023

Cited by 9 | Viewed by 4004

Abstract

The fat mass and obesity-associated (FTO) gene was the first obesity-susceptibility gene identified through a genome-wide association study (GWAS). A growing number of studies have suggested that genetic variants of FTO are strongly associated with the risk of cardiovascular diseases, including [...] Read more.

The fat mass and obesity-associated (FTO) gene was the first obesity-susceptibility gene identified through a genome-wide association study (GWAS). A growing number of studies have suggested that genetic variants of FTO are strongly associated with the risk of cardiovascular diseases, including hypertension and acute coronary syndrome. In addition, FTO was also the first N⁶-methyladenosine (m6A) demethylase, suggesting the reversible nature of m6A modification. m6A is dynamically deposited, removed, and recognized by m6A methylases, demethylases, and m6A binding proteins, respectively. By catalyzing m6A demethylation on mRNA, FTO may participate in various biological processes by modulating RNA function. Recent studies demonstrated that FTO plays a pivotal role in the initiation and progression of cardiovascular diseases such as myocardial fibrosis, heart failure, and atherosclerosis and may hold promise as a potential therapeutic target for treating or preventing a variety of cardiovascular diseases. Here, we review the association between FTO genetic variants and cardiovascular disease risk, summarize the role of FTO as an m6A demethylase in cardiovascular disorders, and discuss future research directions and possible clinical implications. Full article

(This article belongs to the Topic Molecular and Cellular Mechanisms of Diseases: Heart Disease)

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15 pages, 841 KiB  

Open AccessReview

The Intriguing Role of Hypoxia-Inducible Factor in Myocardial Ischemia and Reperfusion: A Comprehensive Review

by Ka-Lin Heck-Swain and Michael Koeppen

J. Cardiovasc. Dev. Dis. 2023, 10(5), 215; https://doi.org/10.3390/jcdd10050215 - 14 May 2023

Cited by 4 | Viewed by 2465

Abstract

Hypoxia-inducible factors (HIFs) play a crucial role in cellular responses to low oxygen levels during myocardial ischemia and reperfusion injury. HIF stabilizers, originally developed for treating renal anemia, may offer cardiac protection in this context. This narrative review examines the molecular mechanisms governing [...] Read more.

Hypoxia-inducible factors (HIFs) play a crucial role in cellular responses to low oxygen levels during myocardial ischemia and reperfusion injury. HIF stabilizers, originally developed for treating renal anemia, may offer cardiac protection in this context. This narrative review examines the molecular mechanisms governing HIF activation and function, as well as the pathways involved in cell protection. Furthermore, we analyze the distinct cellular roles of HIFs in myocardial ischemia and reperfusion. We also explore potential therapies targeting HIFs, emphasizing their possible benefits and limitations. Finally, we discuss the challenges and opportunities in this research area, underscoring the need for continued investigation to fully realize the therapeutic potential of HIF modulation in managing this complex condition. Full article

(This article belongs to the Topic Molecular and Cellular Mechanisms of Diseases: Heart Disease)

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17 pages, 2775 KiB  

Open AccessArticle

Genetic Ablation of Ankrd1 Mitigates Cardiac Damage during Experimental Autoimmune Myocarditis in Mice

by Ieva Rinkūnaitė, Egidijus Šimoliūnas, Milda Alksnė, Gabrielė Bartkutė, Siegfried Labeit, Virginija Bukelskienė and Julius Bogomolovas

Biomolecules 2022, 12(12), 1898; https://doi.org/10.3390/biom12121898 - 18 Dec 2022

Cited by 1 | Viewed by 2477

Abstract

Myocarditis (MC) is an inflammatory disease of the myocardium that can cause sudden death in the acute phase, and dilated cardiomyopathy (DCM) with chronic heart failure as its major long-term outcome. However, the molecular mechanisms beyond the acute MC phase remain poorly understood. [...] Read more.

Myocarditis (MC) is an inflammatory disease of the myocardium that can cause sudden death in the acute phase, and dilated cardiomyopathy (DCM) with chronic heart failure as its major long-term outcome. However, the molecular mechanisms beyond the acute MC phase remain poorly understood. The ankyrin repeat domain 1 (ANKRD1) is a functionally pleiotropic stress/stretch-inducible protein, which can modulate cardiac stress response during various forms of pathological stimuli; however, its involvement in post-MC cardiac remodeling leading to DCM is not known. To address this, we induced experimental autoimmune myocarditis (EAM) in ANKRD1-deficient mice, and evaluated post-MC consequences at the DCM stage mice hearts. We demonstrated that ANKRD1 does not significantly modulate heart failure; nevertheless, the genetic ablation of Ankrd1 blunted the cardiac damage/remodeling and preserved heart function during post-MC DCM. Full article

(This article belongs to the Topic Molecular and Cellular Mechanisms of Diseases: Heart Disease)

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16 pages, 14080 KiB  

Open AccessArticle

The N-Terminal Part of the 1A Domain of Desmin Is a Hot Spot Region for Putative Pathogenic DES Mutations Affecting Filament Assembly

by Andreas Brodehl, Stephanie Holler, Jan Gummert and Hendrik Milting

Cells 2022, 11(23), 3906; https://doi.org/10.3390/cells11233906 - 2 Dec 2022

Cited by 9 | Viewed by 2123

Abstract

Desmin is the major intermediate filament protein of all three muscle cell types, and connects different cell organelles and multi-protein complexes such as the cardiac desmosomes. Several pathogenic mutations in the DES gene cause different skeletal and cardiac myopathies. However, the significance of [...] Read more.

Desmin is the major intermediate filament protein of all three muscle cell types, and connects different cell organelles and multi-protein complexes such as the cardiac desmosomes. Several pathogenic mutations in the DES gene cause different skeletal and cardiac myopathies. However, the significance of the majority of DES missense variants is currently unknown, since functional data are lacking. To determine whether desmin missense mutations within the highly conserved 1A coil domain cause a filament assembly defect, we generated a set of variants with unknown significance and systematically analyzed the filament assembly using confocal microscopy in transfected SW-13, H9c2 cells and cardiomyocytes derived from induced pluripotent stem cells. We found that mutations in the N-terminal part of the 1A coil domain affect filament assembly, leading to cytoplasmic desmin aggregation. In contrast, mutant desmin in the C-terminal part of the 1A coil domain forms filamentous structures comparable to wild-type desmin. Our findings suggest that the N-terminal part of the 1A coil domain is a hot spot for pathogenic desmin mutations, which affect desmin filament assembly. This study may have relevance for the genetic counselling of patients carrying variants in the 1A coil domain of the DES gene. Full article

(This article belongs to the Topic Molecular and Cellular Mechanisms of Diseases: Heart Disease)

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17 pages, 1322 KiB  

Open AccessReview

The Role of Macrophage Iron Overload and Ferroptosis in Atherosclerosis

by Jiedong Ma, Hongqi Zhang, Yufei Chen, Xiaojin Liu, Jiamin Tian and Wei Shen

Biomolecules 2022, 12(11), 1702; https://doi.org/10.3390/biom12111702 - 18 Nov 2022

Cited by 30 | Viewed by 4712

Abstract

Ferroptosis is a new type of cell death caused by iron-dependent lipid peroxidation. In recent years, it has been found that ferroptosis can promote the progression of atherosclerosis (AS). Macrophages have been proven to play multiple roles in the occurrence and development of [...] Read more.

Ferroptosis is a new type of cell death caused by iron-dependent lipid peroxidation. In recent years, it has been found that ferroptosis can promote the progression of atherosclerosis (AS). Macrophages have been proven to play multiple roles in the occurrence and development of AS. Iron is a necessary mineral that participates in different functions of macrophages under physiological conditions. But iron overload and ferroptosis in macrophages may promote the progression of AS. Herein, we summarize the role of iron overload and ferroptosis in macrophages in AS from the perspective of iron metabolism, and iron overload and ferroptosis are significant contributors to AS development. Full article

(This article belongs to the Topic Molecular and Cellular Mechanisms of Diseases: Heart Disease)

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