Search for Articles:
Title / Keyword
Author / Affiliation / Email
Journal
Article Type
 
 
Advanced Search
 
Section
Special Issue
Volume
Issue
Number
Page
 
9.4
4.8
Journals
Biomolecules
Special Issues
Molecular Basis of Cardiac Fibrotic Remodeling: Prognosis of Fibrosis in...
share announcement

Molecular Basis of Cardiac Fibrotic Remodeling: Prognosis of Fibrosis in the Heart

A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Molecular Biology".

Deadline for manuscript submissions: closed (20 October 2024) | Viewed by 9136

Special Issue Editors

Dr. Zhuqiu Jin

E-Mail Website
Guest Editor
Department of Pharmaceutical & Biomedical Sciences, College of Pharmacy, California Northstate University, Elk Grove, CA 95757, USA
Interests: sphingolipids; sphingosine 1-phosphate; PKC theta; ischemic heart injury; cardiac fibrosis; diabetic cardiomyopathy
Dr. Stelios Psarras

E-Mail Website
Guest Editor
Center of Basic Research, Biomedical Research Foundation Academy of Athens, 115 27 Athens, Greece
Interests: tissue inflammation and remodeling; macrophage-fibroblast cross talk; heart failure; cardiac regeneration; cardiopulmonary interactions; fibrosis; airway remodeling and asthma; infectious diseases

Special Issue Information

Dear Colleagues,

Cardiac fibrosis is a pathological process with excessive secretions and deposits of extracellular matrix proteins such as collages, elastin, proteoglycans, and fibronectin. The differentiation of fibroblasts to myofibroblasts is recognized as a critical process in fibrosis. Transforming growth factor beat (TGF-β) promotes this process through Smad-2/3-dependent or -independent pathways. Cellular sources and molecular mechanisms that regulate TGF-β production and function remain incompletely understood.

Atrial fibrotic remodeling is associated with atrial fibrillation. Expansion and dilatation of ventricles result in cardiac remodeling and eventual heart failure. Fibrotic remodeling is one of the major features of cardiac remodeling. Molecules that prevent or ameliorate cardiac fibrosis may be novel targets for chronic heart failure, coronary artery disease, diabetic cardiomyopathy, or other heart disease.

The aim of this Special Issue on Molecular Basis of Cardiac Fibrotic Remodeling is to highlight recent advances of molecules with definitive mechanisms of cardiac fibrosis and remodeling. Investigators of fibrotic remodeling of the heart are especially encouraged to submit. 

Dr. Zhuqiu Jin
Dr. Stelios Psarras
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. Biomolecules 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

  • cardiac fibrosis
  • atrial fibrotic remodeling
  • cardiac repair
  • extracellular matrix remodeling
  • differentiation of fibroblasts to myofibroblasts
  • activation of cardiac fibroblasts

Benefits of Publishing in a Special Issue

  • Ease of navigation: Grouping papers by topic helps scholars navigate broad scope journals more efficiently.
  • Greater discoverability: Special Issues support the reach and impact of scientific research. Articles in Special Issues are more discoverable and cited more frequently.
  • Expansion of research network: Special Issues facilitate connections among authors, fostering scientific collaborations.
  • External promotion: Articles in Special Issues are often promoted through the journal's social media, increasing their visibility.
  • e-Book format: Special Issues with more than 10 articles can be published as dedicated e-books, ensuring wide and rapid dissemination.

Further information on MDPI's Special Issue polices can be found here.

Published Papers (5 papers)

Download All Papers
Order results
Result details
Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:

Research

Jump to: Review

23 pages, 652 KiB  
Article
Fibroblast-Specific Protein-Protein Interactions for Myocardial Fibrosis from MetaCore Network
by Klaus M. Frahm, Ekaterina Kotelnikova, Oksana Kunduzova and Dima L. Shepelyansky
Biomolecules 2024, 14(11), 1395; https://doi.org/10.3390/biom14111395 - 31 Oct 2024
Viewed by 580
Abstract
Myocardial fibrosis is a major pathologic disorder associated with a multitude of cardiovascular diseases (CVD). The pathogenesis is complex and encompasses multiple molecular pathways. Integration of fibrosis-associated genes into the global MetaCore network of protein-protein interactions (PPI) offers opportunities to identify PPI with [...] Read more.
Myocardial fibrosis is a major pathologic disorder associated with a multitude of cardiovascular diseases (CVD). The pathogenesis is complex and encompasses multiple molecular pathways. Integration of fibrosis-associated genes into the global MetaCore network of protein-protein interactions (PPI) offers opportunities to identify PPI with functional and therapeutic significance. Here, we report the generation of a fibrosis-focused PPI network and identification of fibroblast-specific arbitrators driving reparative and reactive myocardial fibrosis. In TGF-β-mediated fibroblast activation, developed network analysis predicts new regulatory mechanisms for fibrosis-associated genes. We introduce an efficient Erdös barrage approach to suppress activation of a number of fibrosis-associated nodes in order to reverse fibrotic cascades. In the network model each protein node is characterized by an Ising up or down spin corresponding to activated or repairing state acting on other nodes being initially in a neutral state. An asynchronous Monte Carlo process describes fibrosis progression determined by a dominant action of linked proteins. Our results suggest that the constructed Ising Network Fibrosis Interaction model offers network insights into fibrosis mechanisms and can complement future experimental efforts to counteract cardiac fibrosis. Full article
(This article belongs to the Special Issue Molecular Basis of Cardiac Fibrotic Remodeling: Prognosis of Fibrosis in the Heart)
►▼ Show Figures

Figure 1

19 pages, 10697 KiB  
Article
PFKFB3 Inhibitor 3PO Reduces Cardiac Remodeling after Myocardial Infarction by Regulating the TGF-β1/SMAD2/3 Pathway
by Qian Yang, Xiao Zong, Lingfang Zhuang, Roubai Pan, Xierenayi Tudi, Qin Fan and Rong Tao
Biomolecules 2023, 13(7), 1072; https://doi.org/10.3390/biom13071072 - 3 Jul 2023
Cited by 2 | Viewed by 2292
Abstract
Adverse cardiac remodeling, including cardiac fibrosis, after myocardial infarction (MI) is a major cause of long-term heart failure. 6-phosphofructo-2-kinase/fructose-2,6-biphosphatase 3 (PFKFB3), an enzyme that regulates glucose metabolism, also plays an important role in various fibrotic and cardiovascular diseases. However, its effects on MI [...] Read more.
Adverse cardiac remodeling, including cardiac fibrosis, after myocardial infarction (MI) is a major cause of long-term heart failure. 6-phosphofructo-2-kinase/fructose-2,6-biphosphatase 3 (PFKFB3), an enzyme that regulates glucose metabolism, also plays an important role in various fibrotic and cardiovascular diseases. However, its effects on MI remain unknown. Here, PFKFB3 inhibitor 3-(3-pyridinyl)-1-(4-pyridinyl)-2-propen-1-one (3PO) and a permanent left anterior descending ligation mouse model were used to explore the functional role of PFKFB3 in MI. We showed that PFKFB3 expression increased significantly in the area of cardiac infarction during the early phase after MI, peaking on day 3. 3PO treatment markedly improved cardiac function, accompanied by decreased infarction size and collagen density in the infarct area. Meanwhile, 3PO attenuated cardiac fibrosis after MI by reducing the expression of collagen and fibronectin in murine hearts. Notably, 3PO reduced PFKFB3 expression and inhibited the transforming growth factor-beta 1/mothers against the decapentaplegic homolog 2/3 (TGF-β1/SMAD2/3) signaling pathway to inhibit cardiac fibrosis after MI. Moreover, PFKFB3 expression in neonatal rat cardiac fibroblasts (NRCFs) increased significantly after MI and under hypoxia, whereas 3PO alleviated the migratory capacity and activation of NRCFs induced by TGF-β1. In conclusion, 3PO effectively reduced fibrosis and improved adverse cardiac remodeling after MI, suggesting PFKFB3 inhibition as a novel therapeutic strategy to reduce the incidence of chronic heart failure following MI. Full article
(This article belongs to the Special Issue Molecular Basis of Cardiac Fibrotic Remodeling: Prognosis of Fibrosis in the Heart)
►▼ Show Figures

Graphical abstract

Review

Jump to: Research

35 pages, 2305 KiB  
Review
The Macrophage–Fibroblast Dipole in the Context of Cardiac Repair and Fibrosis
by Stelios Psarras
Biomolecules 2024, 14(11), 1403; https://doi.org/10.3390/biom14111403 - 4 Nov 2024
Viewed by 676
Abstract
Stromal and immune cells and their interactions have gained the attention of cardiology researchers and clinicians in recent years as their contribution in cardiac repair is increasingly recognized. The repair process in the heart is a particularly critical constellation of complex molecular and [...] Read more.
Stromal and immune cells and their interactions have gained the attention of cardiology researchers and clinicians in recent years as their contribution in cardiac repair is increasingly recognized. The repair process in the heart is a particularly critical constellation of complex molecular and cellular events and interactions that characteristically fail to ensure adequate recovery following injury, insult, or exposure to stress conditions in this regeneration-hostile organ. The tremendous consequence of this pronounced inability to maintain homeostatic states is being translated in numerous ways promoting progress into heart failure, a deadly, irreversible condition requiring organ transplantation. Fibrosis is in fact a repair response eventually promoting cardiac dysfunction and cardiac fibroblasts are the major cellular players in this process, overproducing collagens and other extracellular matrix components when activated. On the other hand, macrophages may differentially affect fibroblasts and cardiac repair depending on their status and subsets. The opposite interaction is also probable. We discuss here the multifaceted aspects and crosstalk of this cell dipole and the opportunities it may offer for beneficial manipulation approaches that will hopefully lead to progress in heart disease interventions. Full article
(This article belongs to the Special Issue Molecular Basis of Cardiac Fibrotic Remodeling: Prognosis of Fibrosis in the Heart)
►▼ Show Figures

Figure 1

21 pages, 1395 KiB  
Review
Novel Biomarkers and Advanced Cardiac Imaging in Aortic Stenosis: Old and New
by Anca Drăgan and Anca Doina Mateescu
Biomolecules 2023, 13(11), 1661; https://doi.org/10.3390/biom13111661 - 17 Nov 2023
Viewed by 1691
Abstract
Currently, the symptomatic status and left ventricular ejection fraction (LVEF) play a crucial role in aortic stenosis (AS) assessment. However, the symptoms are often subjective, and LVEF is not a sensitive marker of left ventricle (LV) decompensation. Over the past years, the cardiac [...] Read more.
Currently, the symptomatic status and left ventricular ejection fraction (LVEF) play a crucial role in aortic stenosis (AS) assessment. However, the symptoms are often subjective, and LVEF is not a sensitive marker of left ventricle (LV) decompensation. Over the past years, the cardiac structure and function research on AS has increased due to advanced imaging modalities and potential therapies. New imaging parameters emerged as predictors of disease progression in AS. LV global longitudinal strain has proved useful for risk stratification in asymptomatic severe AS patients with preserved LVEF. The assessment of myocardial fibrosis by cardiac magnetic resonance is the most studied application and offers prognostic information on AS. Moreover, the usage of biomarkers in AS as objective measures of LV decompensation has recently gained more interest. The present review focuses on the transition from compensatory LV hypertrophy (H) to LV dysfunction and the biomarkers associated with myocardial wall stress, fibrosis, and myocyte death. Moreover, we discuss the potential impact of non-invasive imaging parameters for optimizing the timing of aortic valve replacement and provide insight into novel biomarkers for possible prognostic use in AS. However, data from randomized clinical trials are necessary to define their utility in daily practice. Full article
(This article belongs to the Special Issue Molecular Basis of Cardiac Fibrotic Remodeling: Prognosis of Fibrosis in the Heart)
►▼ Show Figures

Figure 1

29 pages, 3166 KiB  
Review
Mitochondrial Calcium Overload Plays a Causal Role in Oxidative Stress in the Failing Heart
by Haikel Dridi, Gaetano Santulli, Laith Bahlouli, Marco C. Miotto, Gunnar Weninger and Andrew R. Marks
Biomolecules 2023, 13(9), 1409; https://doi.org/10.3390/biom13091409 - 19 Sep 2023
Cited by 6 | Viewed by 2912
Abstract
Heart failure is a serious global health challenge, affecting more than 6.2 million people in the United States and is projected to reach over 8 million by 2030. Independent of etiology, failing hearts share common features, including defective calcium (Ca2+) handling, [...] Read more.
Heart failure is a serious global health challenge, affecting more than 6.2 million people in the United States and is projected to reach over 8 million by 2030. Independent of etiology, failing hearts share common features, including defective calcium (Ca2+) handling, mitochondrial Ca2+ overload, and oxidative stress. In cardiomyocytes, Ca2+ not only regulates excitation–contraction coupling, but also mitochondrial metabolism and oxidative stress signaling, thereby controlling the function and actual destiny of the cell. Understanding the mechanisms of mitochondrial Ca2+ uptake and the molecular pathways involved in the regulation of increased mitochondrial Ca2+ influx is an ongoing challenge in order to identify novel therapeutic targets to alleviate the burden of heart failure. In this review, we discuss the mechanisms underlying altered mitochondrial Ca2+ handling in heart failure and the potential therapeutic strategies. Full article
(This article belongs to the Special Issue Molecular Basis of Cardiac Fibrotic Remodeling: Prognosis of Fibrosis in the Heart)
►▼ Show Figures

Figure 1

Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:
 
Displaying articles 1-5
Back to TopTop