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Cells
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Cellular Signaling Leading to Heart Failure
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Cellular Signaling Leading to Heart Failure

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

Deadline for manuscript submissions: closed (31 July 2022) | Viewed by 19569

Special Issue Editors

Dr. Paula A. Da Costa-Martins

E-Mail Website
Guest Editor
Cardiovascular Research Institute Maastricht, Medicine and Life Sciences, Maastricht, The Netherlands
Interests: cardiovascular genetics; microRNA; ncRNAs
Dr. Frank Lezoualc’h

E-Mail Website
Guest Editor
Inserm Institut national de la santé et de la recherche médicale, Toulouse, France
Interests: molecular pharmacology; camp; physiology, cell signalling; cardiovascular diseases

Special Issue Information

Dear Colleagues, 

Heart failure (HF) is among the leading causes of death worldwide, with an increased prevalence in the elderly. HF derives from various different diseases, such as hypertension, myocardial infarction, as well as metabolic and genetic disorders. This syndrome is generally preceded by remodeling processes that include myocardial hypertrophy, fibrosis, inflammation, vascular dysfunction, and cardiomyocyte death, leading progressively to cardiac dysfunction and rhythm alterations. Although current therapies targeting ventricular remodeling are effective in reducing morbidity and mortality, mostly in patients with systolic heart failure (HF with reduced ejection fraction, HFrEF), in many instances disease progression continues unabated. No treatment is yet available for patients with HF with preserved ejection fraction (HFpEF),  representing  more than 50% of the prevalent HF cases. Thus, understanding the mechanisms that regulate cardiac remodeling processes might pave the way to important scientific and therapeutic developments in HF.

This Special Issue of Cells is devoted to summarizing current knowledge on the molecular events underlying pathological cardiac remodeling in HFrEF and/or HFpEF. We seek the submission of articles and review papers on topics including, but not limited to, epigenetic mechanisms, membrane receptor and kinase signaling, calcium alterations, mitochondrial dysfunction, remodeling and metabolic dysregulation leading to adverse remodeling and HF, and the identification of new therapeutic targets.

We look forward to your contributions.

Dr. Paula A. Da Costa-Martins
Dr. Frank Lezoualc’h
Guest Editors

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.

Keywords

  • Cardiac remodeling
  • heart failure
  • epigenetics
  • mitochondria
  • cardiac metabolism
  • calcium, signaling
  • transcriptional/post-transcriptional regulation
  • cardiac intercellular communication

Published Papers (6 papers)

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Research

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23 pages, 3340 KiB  
Article
Monoamine Oxidase-Dependent Pro-Survival Signaling in Diabetic Hearts Is Mediated by miRNAs
by Stefano Cagnin, Marco Brugnaro, Caterina Millino, Beniamina Pacchioni, Carmen Troiano, Moises Di Sante and Nina Kaludercic
Cells 2022, 11(17), 2697; https://doi.org/10.3390/cells11172697 - 30 Aug 2022
Cited by 9 | Viewed by 2285
Abstract
Diabetes leads to cardiomyopathy and heart failure, the leading cause of death for diabetic patients. Monoamine oxidase (MAO) inhibition in diabetic cardiomyopathy prevents oxidative stress, mitochondrial and endoplasmic reticulum stress and the development of diastolic dysfunction. However, it is unclear whether, in addition [...] Read more.
Diabetes leads to cardiomyopathy and heart failure, the leading cause of death for diabetic patients. Monoamine oxidase (MAO) inhibition in diabetic cardiomyopathy prevents oxidative stress, mitochondrial and endoplasmic reticulum stress and the development of diastolic dysfunction. However, it is unclear whether, in addition to the direct effects exerted on the mitochondria, MAO activity is able to post-transcriptionally regulate cardiomyocyte function and survival in diabetes. To this aim, we performed gene and miRNA expression profiling in cardiac tissue from streptozotocin-treated mice (model of type 1 diabetes (T1D)), administered with either vehicle or MAOs inhibitor pargyline for 12 weeks. We found that inhibition of MAO activity in T1D hearts leads to profound transcriptomic changes, affecting autophagy and pro-survival pathways activation. MAO activity in T1D hearts increased miR-133a-3p, -193a-3p and -27a-3p expression. These miRNAs target insulin-like growth factor receptor 1 (Igf1r), growth factor receptor bound protein 10 and inositol polyphosphate 4 phosphatase type 1A, respectively, all components of the IGF1R/PI3K/AKT signaling pathway. Indeed, AKT activation was significantly downregulated in T1D hearts, whereas MAO inhibition restored the activation of this pro-survival pathway. The present study provides an important link between MAO activity, transcriptomic changes and activation of pro-survival signaling and autophagy in diabetic cardiomyopathy. Full article
(This article belongs to the Special Issue Cellular Signaling Leading to Heart Failure)
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27 pages, 2888 KiB  
Article
MSK-Mediated Phosphorylation of Histone H3 Ser28 Couples MAPK Signalling with Early Gene Induction and Cardiac Hypertrophy
by Emma L. Robinson, Faye M. Drawnel, Saher Mehdi, Caroline R. Archer, Wei Liu, Hanneke Okkenhaug, Kanar Alkass, Jan Magnus Aronsen, Chandan K. Nagaraju, Ivar Sjaastad, Karin R. Sipido, Olaf Bergmann, J. Simon C. Arthur, Xin Wang and H. Llewelyn Roderick
Cells 2022, 11(4), 604; https://doi.org/10.3390/cells11040604 - 09 Feb 2022
Cited by 7 | Viewed by 3042
Abstract
Heart failure is a leading cause of death that develops subsequent to deleterious hypertrophic cardiac remodelling. MAPK pathways play a key role in coordinating the induction of gene expression during hypertrophy. Induction of the immediate early gene (IEG) response including activator protein 1 [...] Read more.
Heart failure is a leading cause of death that develops subsequent to deleterious hypertrophic cardiac remodelling. MAPK pathways play a key role in coordinating the induction of gene expression during hypertrophy. Induction of the immediate early gene (IEG) response including activator protein 1 (AP-1) complex factors is a necessary and early event in this process. How MAPK and IEG expression are coupled during cardiac hypertrophy is not resolved. Here, in vitro, in rodent models and in human samples, we demonstrate that MAPK-stimulated IEG induction depends on the mitogen and stress-activated protein kinase (MSK) and its phosphorylation of histone H3 at serine 28 (pH3S28). pH3S28 in IEG promoters in turn recruits Brg1, a BAF60 ATP-dependent chromatin remodelling complex component, initiating gene expression. Without MSK activity and IEG induction, the hypertrophic response is suppressed. These studies provide new mechanistic insights into the role of MAPK pathways in signalling to the epigenome and regulation of gene expression during cardiac hypertrophy. Full article
(This article belongs to the Special Issue Cellular Signaling Leading to Heart Failure)
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9 pages, 1052 KiB  
Article
Circulating miR-185-5p as a Potential Biomarker for Arrhythmogenic Right Ventricular Cardiomyopathy
by Claudia Sacchetto, Zenab Mohseni, Robin M. W. Colpaert, Libero Vitiello, Marzia De Bortoli, Indira G. C. Vonhögen, Ke Xiao, Giulia Poloni, Alessandra Lorenzon, Chiara Romualdi, Riccardo Bariani, Elisa Mazzotti, Luciano Daliento, Barbara Bauce, Domenico Corrado, Thomas Thum, Alessandra Rampazzo, Leon J. de Windt and Martina Calore
Cells 2021, 10(10), 2578; https://doi.org/10.3390/cells10102578 - 28 Sep 2021
Cited by 8 | Viewed by 2283
Abstract
Arrhythmogenic right ventricular cardiomyopathy (ARVC) is a genetic cardiac disease characterized by progressive myocardial fibro-fatty replacement, arrhythmias and risk of sudden death. Its diagnosis is challenging and often it is achieved after disease onset or postmortem. In this study, we sought to identify [...] Read more.
Arrhythmogenic right ventricular cardiomyopathy (ARVC) is a genetic cardiac disease characterized by progressive myocardial fibro-fatty replacement, arrhythmias and risk of sudden death. Its diagnosis is challenging and often it is achieved after disease onset or postmortem. In this study, we sought to identify circulating microRNAs (miRNAs) differentially expressed in ARVC patients compared to healthy controls. In the pilot study, we screened the expression of 754 miRNAs from 21 ARVC patients and 20 healthy controls. After filtering the miRNAs considering a log fold-change cut-off of ±1, p-value < 0.05, we selected five candidate miRNAs for a subsequent validation study in which we used TaqMan-based real-time PCR to analyse samples from 37 ARVC patients and 30 healthy controls. We found miR-185-5p significantly upregulated in ARVC patients. Receiver operating characteristic analysis indicated an area under the curve of 0.854, corroborating the link of this miRNA and ARVC pathophysiology. Full article
(This article belongs to the Special Issue Cellular Signaling Leading to Heart Failure)
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Review

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15 pages, 1064 KiB  
Review
Calcium-Sensing Receptor (CaSR)-Mediated Intracellular Communication in Cardiovascular Diseases
by Hezhen Chu, Zhenqian Qin, Jun Ma, Yimin Xie, Haifeng Shi, Jie Gu and Baiqiang Shi
Cells 2022, 11(19), 3075; https://doi.org/10.3390/cells11193075 - 30 Sep 2022
Cited by 1 | Viewed by 3553
Abstract
The calcium-sensing receptor (CaSR), a G-protein-coupled receptor (GPCR), is a cell-surface-located receptor that can induce highly diffusible messengers (IP3, Ca2+, cAMP) in the cytoplasm to activate various cellular responses. Recently, it has also been suggested that the CaSR mediates the intracellular [...] Read more.
The calcium-sensing receptor (CaSR), a G-protein-coupled receptor (GPCR), is a cell-surface-located receptor that can induce highly diffusible messengers (IP3, Ca2+, cAMP) in the cytoplasm to activate various cellular responses. Recently, it has also been suggested that the CaSR mediates the intracellular communications between the endoplasmic reticulum (ER), mitochondria, nucleus, protease/proteasome, and autophagy–lysosome, which are involved in related cardiovascular diseases. The complex intracellular signaling of this receptor challenges it as a valuable therapeutic target. It is, therefore, necessary to understand the mechanisms behind the signaling characteristics of this receptor in intracellular communication. This review provides an overview of the recent research progress on the various regulatory mechanisms of the CaSR in related cardiovascular diseases and the heart–kidney interaction; the associated common causes are also discussed. Full article
(This article belongs to the Special Issue Cellular Signaling Leading to Heart Failure)
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25 pages, 822 KiB  
Review
Non-Coding RNAs in the Therapeutic Landscape of Pathological Cardiac Hypertrophy
by Joana Silva and Paula A. da Costa Martins
Cells 2022, 11(11), 1805; https://doi.org/10.3390/cells11111805 - 31 May 2022
Cited by 3 | Viewed by 3121
Abstract
Cardiovascular diseases are a major health problem, and long-term survival for people diagnosed with heart failure is, still, unrealistic. Pathological cardiac hypertrophy largely contributes to morbidity and mortality, as effective therapeutic approaches are lacking. Non-coding RNAs (ncRNAs) arise as active regulators of the [...] Read more.
Cardiovascular diseases are a major health problem, and long-term survival for people diagnosed with heart failure is, still, unrealistic. Pathological cardiac hypertrophy largely contributes to morbidity and mortality, as effective therapeutic approaches are lacking. Non-coding RNAs (ncRNAs) arise as active regulators of the signaling pathways and mechanisms that govern this pathology, and their therapeutic potential has received great attention in the last decades. Preclinical studies in large animal models have been successful in ameliorating cardiac hypertrophy, and an antisense drug for the treatment of heart failure has, already, entered clinical trials. In this review, we provide an overview of the molecular mechanisms underlying cardiac hypertrophy, the involvement of ncRNAs, and the current therapeutic landscape of oligonucleotides targeting these regulators. Strategies to improve the delivery of such therapeutics and overcome the actual challenges are, also, defined and discussed. With the fast advance in the improvement of oligonucleotide drug delivery, the inclusion of ncRNAs-targeting therapies for cardiac hypertrophy seems, increasingly, a closer reality. Full article
(This article belongs to the Special Issue Cellular Signaling Leading to Heart Failure)
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26 pages, 2589 KiB  
Review
Early Protective Role of Inflammation in Cardiac Remodeling and Heart Failure: Focus on TNFα and Resident Macrophages
by Sophie Besse, Sophie Nadaud, Elise Balse and Catherine Pavoine
Cells 2022, 11(7), 1249; https://doi.org/10.3390/cells11071249 - 06 Apr 2022
Cited by 21 | Viewed by 4470
Abstract
Cardiac hypertrophy, initiated by a variety of physiological or pathological stimuli (hemodynamic or hormonal stimulation or infarction), is a critical early adaptive compensatory response of the heart. The structural basis of the progression from compensated hypertrophy to pathological hypertrophy and heart failure is [...] Read more.
Cardiac hypertrophy, initiated by a variety of physiological or pathological stimuli (hemodynamic or hormonal stimulation or infarction), is a critical early adaptive compensatory response of the heart. The structural basis of the progression from compensated hypertrophy to pathological hypertrophy and heart failure is still largely unknown. In most cases, early activation of an inflammatory program reflects a reparative or protective response to other primary injurious processes. Later on, regardless of the underlying etiology, heart failure is always associated with both local and systemic activation of inflammatory signaling cascades. Cardiac macrophages are nodal regulators of inflammation. Resident macrophages mostly attenuate cardiac injury by secreting cytoprotective factors (cytokines, chemokines, and growth factors), scavenging damaged cells or mitochondrial debris, and regulating cardiac conduction, angiogenesis, lymphangiogenesis, and fibrosis. In contrast, excessive recruitment of monocyte-derived inflammatory macrophages largely contributes to the transition to heart failure. The current review examines the ambivalent role of inflammation (mainly TNFα-related) and cardiac macrophages (Mφ) in pathophysiologies from non-infarction origin, focusing on the protective signaling processes. Our objective is to illustrate how harnessing this knowledge could pave the way for innovative therapeutics in patients with heart failure. Full article
(This article belongs to the Special Issue Cellular Signaling Leading to Heart Failure)
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