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Cardiac Fibrosis and Remodeling
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Cardiac Fibrosis and Remodeling

A special issue of Journal of Cardiovascular Development and Disease (ISSN 2308-3425). This special issue belongs to the section "Cardiac Development and Regeneration".

Deadline for manuscript submissions: closed (30 November 2023) | Viewed by 8642

Special Issue Editor

Prof. Dr. Kishore Pasumarthi

E-Mail Website
Guest Editor
Department of Pharmacology, Dalhousie University, Halifax, NS B3H 4R2, Canada
Interests: cardiac progenitor cells; ventricular conduction system development; natriuretic peptide receptor signaling; myocardial repair; cardiac fibrosis and remodeling; cell transplantation; cardiomyocyte cell cycle regulation

Special Issue Information

Dear Colleagues,

Cardiac fibrosis is an underlying pathology in many forms of heart disease and is known to result from an imbalance in the synthesis and degradation of the myocardial extracellular matrix (ECM) and tissue remodeling. Chronic myocardial fibrosis is a poor prognostic sign that is known to cause diastolic and systolic dysfunction and increase susceptibility of the heart to arrhythmias leading to heart failure. Several studies have underscored the importance of cardiac fibroblasts in ECM synthesis and remodeling during normal heart development and disease states. There is a growing body of knowledge on topics including but not limited to lineage tracing of cardiac fibroblasts, phenotype conversion of fibroblasts into myofibroblasts, mediators and signal transduction pathways regulating fibrosis, the role of microRNAs and pharmacological agents in fibrosis, and tissue remodeling. The Special Issue of cardiac fibrosis and remodeling aims to shed light on new models of myocardial fibrosis, emerging fibrosis pathways, biomarkers, detection methodologies, the role of immune system and metabolic pathways, and genetic and pharmacological interventions as well as limitations and challenges for the translation of mechanistic knowledge into the clinic.

Prof. Dr. Kishore Pasumarthi
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. Journal of Cardiovascular Development and Disease is an international peer-reviewed open access monthly 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

  • animal models of cardiac fibrosis
  • mediators and signaling pathways
  • biomarkers and detection methodologies
  • extracellular matrix remodeling mechanisms
  • immune system and metabolic pathways
  • genetic and pharmacological interventions
  • translational approaches

Published Papers (4 papers)

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Research

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17 pages, 9589 KiB  
Article
A Mouse Model of Dilated Cardiomyopathy Produced by Isoproterenol Acute Exposure Followed by 5-Fluorouracil Administration
by Nadia Salerno, Mariangela Scalise, Fabiola Marino, Andrea Filardo, Antonio Chiefalo, Giuseppe Panuccio, Michele Torella, Antonella De Angelis, Salvatore De Rosa, Georgina M. Ellison-Hughes, Konrad Urbanek, Giuseppe Viglietto, Daniele Torella and Eleonora Cianflone
J. Cardiovasc. Dev. Dis. 2023, 10(6), 225; https://doi.org/10.3390/jcdd10060225 - 23 May 2023
Cited by 1 | Viewed by 2173
Abstract
Appropriate dilated cardiomyopathy (DCM) animal models are highly desirable considering the pathophysiological and clinical heterogeneity of DCM. Genetically modified mice are the most widely and intensively utilized research animals for DCM. However, to translate discoveries from basic science into new and personalized medical [...] Read more.
Appropriate dilated cardiomyopathy (DCM) animal models are highly desirable considering the pathophysiological and clinical heterogeneity of DCM. Genetically modified mice are the most widely and intensively utilized research animals for DCM. However, to translate discoveries from basic science into new and personalized medical applications, research in non-genetically based DCM models remains a key issue. Here, we characterized a mouse model of non-ischemic DCM induced by a stepwise pharmacologic regime of Isoproterenol (ISO) high dose bolus followed by a low dose systemic injection of the chemotherapy agent, 5-Fluorouracil (5-FU). C57BL/6J mice were injected with ISO and, 3 days after, were randomly assigned to saline or 5-FU. Echocardiography and a strain analysis show that ISO + 5FU in mice induces progressive left ventricular (LV) dilation and reduced systolic function, along with diastolic dysfunction and a persistent global cardiac contractility depression through 56 days. While mice treated with ISO alone recover anatomically and functionally, ISO + 5-FU causes persistent cardiomyocyte death, ensuing in cardiomyocyte hypertrophy through 56 days. ISO + 5-FU-dependent damage was accompanied by significant myocardial disarray and fibrosis along with exaggerated oxidative stress, tissue inflammation and premature cell senescence accumulation. In conclusions, a combination of ISO + 5FU produces anatomical, histological and functional cardiac alterations typical of DCM, representing a widely available, affordable, and reproducible mouse model of this cardiomyopathy. Full article
(This article belongs to the Special Issue Cardiac Fibrosis and Remodeling)
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20 pages, 4622 KiB  
Article
Ciclopirox Inhibition of eIF5A Hypusination Attenuates Fibroblast Activation and Cardiac Fibrosis
by Kadiam C. Venkata Subbaiah, Jiangbin Wu, Wai Hong Wilson Tang and Peng Yao
J. Cardiovasc. Dev. Dis. 2023, 10(2), 52; https://doi.org/10.3390/jcdd10020052 - 29 Jan 2023
Cited by 3 | Viewed by 2032
Abstract
Cardiac fibrosis is a primary contributor to heart failure (HF), and is considered to be a targetable process for HF therapy. Cardiac fibroblast (CF) activation accompanied by excessive extracellular matrix (ECM) production is central to the initiation and maintenance of fibrotic scarring in [...] Read more.
Cardiac fibrosis is a primary contributor to heart failure (HF), and is considered to be a targetable process for HF therapy. Cardiac fibroblast (CF) activation accompanied by excessive extracellular matrix (ECM) production is central to the initiation and maintenance of fibrotic scarring in cardiac fibrosis. However, therapeutic compounds targeting CF activation remain limited in treating cardiac fibrosis. Eukaryotic translation initiation factor 5A (eIF5A), upon being hypusinated, is essential for the translation elongation of proline-codon rich mRNAs. In this study, we found that increased hypusinated eIF5A protein levels were associated with cardiac fibrosis and heart dysfunction in myocardial infarction (MI) mouse models. Ciclopirox (CPX), an FDA-approved antifungal drug, inhibits the deoxyhypusine hydroxylase (DOHH) enzyme required for eIF5A hypusination. Results from preventive and reversal mouse models suggest that CPX treatment significantly reduced MI-driven cardiac fibrosis and improved cardiac function. In vitro studies of isolated mouse primary CFs revealed that inhibition of eIF5A hypusination using CPX significantly abolished TGFβ induced CF proliferation, activation, and collagen expression. Proteomic analysis from mouse CFs reveals that CPX downregulates the expression of proline-rich proteins that are enriched in extracellular matrix and cell adhesion pathways. Our findings are relevant to human heart disease, as increased hypusinated eIF5A levels were observed in heart samples of ischemic heart failure patients compared to healthy subjects. Together, these results suggest that CPX can be repurposed to treat cardiac fibrosis and ischemic heart failure. Full article
(This article belongs to the Special Issue Cardiac Fibrosis and Remodeling)
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Review

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29 pages, 9825 KiB  
Review
Bioactive Compounds and Cardiac Fibrosis: Current Insight and Future Prospect
by Abdul Majid, Fasilat Oluwakemi Hassan, Md Monirul Hoque, Joy Olaoluwa Gbadegoye and Djamel Lebeche
J. Cardiovasc. Dev. Dis. 2023, 10(7), 313; https://doi.org/10.3390/jcdd10070313 - 21 Jul 2023
Cited by 1 | Viewed by 2329
Abstract
Cardiac fibrosis is a pathological condition characterized by excessive deposition of collagen and other extracellular matrix components in the heart. It is recognized as a major contributor to the development and progression of heart failure. Despite significant research efforts in characterizing and identifying [...] Read more.
Cardiac fibrosis is a pathological condition characterized by excessive deposition of collagen and other extracellular matrix components in the heart. It is recognized as a major contributor to the development and progression of heart failure. Despite significant research efforts in characterizing and identifying key molecular mechanisms associated with myocardial fibrosis, effective treatment for this condition is still out of sight. In this regard, bioactive compounds have emerged as potential therapeutic antifibrotic agents due to their anti-inflammatory and antioxidant properties. These compounds exhibit the ability to modulate fibrogenic processes by inhibiting the production of extracellular matrix proteins involved in fibroblast to myofibroblast differentiation, or by promoting their breakdown. Extensive investigation of these bioactive compounds offers new possibilities for preventing or reducing cardiac fibrosis and its detrimental consequences. This comprehensive review aims to provide a thorough overview of the mechanisms underlying cardiac fibrosis, address the limitations of current treatment strategies, and specifically explore the potential of bioactive compounds as therapeutic interventions for the treatment and/or prevention of cardiac fibrosis. Full article
(This article belongs to the Special Issue Cardiac Fibrosis and Remodeling)
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Other

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13 pages, 1880 KiB  
Systematic Review
The Influence of IL-11 on Cardiac Fibrosis in Experimental Models: A Systematic Review
by Yarlla Loyane Lira Braga, José Rodrigues do Carmo Neto, Pablo Igor Ribeiro Franco, Fernanda Rodrigues Helmo, Marlene Antônia dos Reis, Flávia Aparecida de Oliveira, Mara Rúbia Nunes Celes, Marcos Vinícius da Silva and Juliana Reis Machado
J. Cardiovasc. Dev. Dis. 2024, 11(2), 65; https://doi.org/10.3390/jcdd11020065 - 17 Feb 2024
Viewed by 1274
Abstract
Fibrosis is one of the main factors that impair the function of many organs. In the heart, fibrosis leads to contractile dysfunction and arrhythmias, which are important in the development of heart failure. Interleukin (IL)-11 is regulated in various heart diseases and has [...] Read more.
Fibrosis is one of the main factors that impair the function of many organs. In the heart, fibrosis leads to contractile dysfunction and arrhythmias, which are important in the development of heart failure. Interleukin (IL)-11 is regulated in various heart diseases and has recently been reported to be an important cytokine in fibrosis in this organ. However, this topic has been little explored, and many questions persist. Thus, this systematic review aimed to report on possible IL-11 therapies evaluated in rodent model-induced cardiac fibrosis. Inclusion criteria were experimental in vivo studies that used different rodent models for cardiac fibrosis associated with IL-11 interventions, without year and language restrictions. The search in PubMed, Web of Science, and Embase databases was performed in October 2022. The risk of bias assessment of the studies was based on the guidelines of the SYRCLE tool, and data from the selected articles were also presented in a table as a narrative description. This review was based on eight studies in which five different interventions were used: recombinant human IL-11 (rhIL-11), anti-IL11 (X203), recombinant mouse IL-11 (rmIL-11), lentivirus (LV)-IL-11 + lutein, and anti-IL11RA (X209). Based on the included studies, the results were variable, with IL-11 overexpression inducing cardiac fibrosis, while inhibition protected against this process, preserving the function of this organ. Therefore, IL-11 stands out as a promising therapeutic target for cardiac fibrosis. However, further studies are needed to understand the mechanisms triggered by each treatment, as well as its safety and immunogenicity. Full article
(This article belongs to the Special Issue Cardiac Fibrosis and Remodeling)
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