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Cardiac Fibroblasts and Fibrosis
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Cardiac Fibroblasts and Fibrosis

A special issue of Journal of Cardiovascular Development and Disease (ISSN 2308-3425).

Deadline for manuscript submissions: closed (31 July 2019) | Viewed by 37028

Special Issue Editor

Prof. Dr. Michelle Tallquist

E-Mail Website
Guest Editor
Center for Cardiovascular Research, BSB311E, 651 Ilalo St, Honolulu, HI 96813, USA
Interests: fibroblasts; Tcf21; PDGF signaling; cardiovascular development; extracellular matrix; inflammation; epicardial cell differentiation

Special Issue Information

Dear colleagues,

The Journal of Cardiovascular Development and Disease announces a Special Issue on cardiac fibroblasts and fibrosis. Cardiac fibrosis is associated with most pathological conditions of the heart, yet few therapeutic strategies have been identified that successfully reduce fibrosis progression. While the cardiac fibroblast has long been appreciated for its contribution to extracellular matrix remodeling after heart injury and during aging, effective mechanisms for curtailing fibroblast expansion and ECM deposition are minimal. One explanation for the lack of treatment options is a relatively poor understanding of the fibroblast and the signaling mechanisms that guide its behavior. Recent studies have provided a better comprehension of cardiac fibroblast gene expression and demonstrated multiple developmental origins, but there remains a need to understand fibroblast diversity after injury with consideration of temporal and spatial distinctions. A deeper understanding of the range of signaling pathways that dictate fibroblast behaviors during homeostasis and after injury is also needed. The aim of this Special Issue is to provide a venue for studies that show an appreciation of the diversity of resident cardiac fibroblast signaling and gene expression during development, cardiac remodeling, and aging.

Prof. Michelle Tallquist
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

  • Fibroblasts
  • Fibrosis
  • Cardiac development
  • Aging
  • Extracellular matrix
  • Ischemia
  • Cardiac remodeling

Published Papers (6 papers)

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Research

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18 pages, 3481 KiB  
Article
Ischemia Reperfusion Injury Produces, and Ischemic Preconditioning Prevents, Rat Cardiac Fibroblast Differentiation: Role of KATP Channels
by Kartika R. Pertiwi, Rachael M. Hillman, Coralie A. Scott and Emily Lisa Chilton
J. Cardiovasc. Dev. Dis. 2019, 6(2), 22; https://doi.org/10.3390/jcdd6020022 - 4 Jun 2019
Cited by 16 | Viewed by 4236
Abstract
Ischemic preconditioning (IPC) and activation of ATP-sensitive potassium channels (KATP) protect cardiac myocytes from ischemia reperfusion (IR) injury. We investigated the influence of IR injury, IPC and KATP in isolated rat cardiac fibroblasts. Hearts were removed under isoflurane anesthesia. IR [...] Read more.
Ischemic preconditioning (IPC) and activation of ATP-sensitive potassium channels (KATP) protect cardiac myocytes from ischemia reperfusion (IR) injury. We investigated the influence of IR injury, IPC and KATP in isolated rat cardiac fibroblasts. Hearts were removed under isoflurane anesthesia. IR was simulated in vitro by application and removal of paraffin oil over pelleted cells. Ischemia (30, 60 and 120 min) followed by 60 min reperfusion resulted in significant differentiation of fibroblasts into myofibroblasts in culture (mean % fibroblasts ± SEM in IR vs. time control: 12 ± 1% vs. 63 ± 2%, 30 min ischemia; 15 ± 3% vs. 71 ± 4%, 60 min ischemia; 8 ± 1% vs. 55 ± 2%, 120 min ischemia). IPC (15 min ischemia, 30 min reperfusion) significantly attenuated IR-induced fibroblast differentiation (52 ± 3%) compared to 60 min IR. IPC was mimicked by opening KATP with pinacidil (50 μM; 43 ± 6%) and by selectively opening mitochondrial KATP (mKATP) with diazoxide (100 μM; 53 ± 3%). Furthermore, IPC was attenuated by inhibiting KATP with glibenclamide (10 μM; 23 ± 5%) and by selectively blocking mKATP with 5-hydroxydecanoate (100 μM; 22 ± 9%). These results suggest that (a) IR injury evoked cardiac fibroblast to myofibroblast differentiation, (b) IPC attenuated IR-induced fibroblast differentiation, (c) KATP were involved in IPC and (d) this protection involved selective activation of mKATP. Full article
(This article belongs to the Special Issue Cardiac Fibroblasts and Fibrosis)
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Review

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24 pages, 1152 KiB  
Review
The Non-Fibrillar Side of Fibrosis: Contribution of the Basement Membrane, Proteoglycans, and Glycoproteins to Myocardial Fibrosis
by Michael Chute, Preetinder Aujla, Sayantan Jana and Zamaneh Kassiri
J. Cardiovasc. Dev. Dis. 2019, 6(4), 35; https://doi.org/10.3390/jcdd6040035 - 23 Sep 2019
Cited by 30 | Viewed by 6272
Abstract
The extracellular matrix (ECM) provides structural support and a microenvironmentfor soluble extracellular molecules. ECM is comprised of numerous proteins which can be broadly classified as fibrillar (collagen types I and III) and non-fibrillar (basement membrane, proteoglycans, and glycoproteins). The basement membrane provides an [...] Read more.
The extracellular matrix (ECM) provides structural support and a microenvironmentfor soluble extracellular molecules. ECM is comprised of numerous proteins which can be broadly classified as fibrillar (collagen types I and III) and non-fibrillar (basement membrane, proteoglycans, and glycoproteins). The basement membrane provides an interface between the cardiomyocytes and the fibrillar ECM, while proteoglycans sequester soluble growth factors and cytokines. Myocardial fibrosis was originally only linked to accumulation of fibrillar collagens, but is now recognized as the expansion of the ECM including the non-fibrillar ECM proteins. Myocardial fibrosis can be reparative to replace the lost myocardium (e.g., ischemic injury or myocardial infarction), or can be reactive resulting from pathological activity of fibroblasts (e.g., dilated or hypertrophic cardiomyopathy). Contribution of fibrillar collagens to fibrosis is well studied, but the role of the non-fibrillar ECM proteins has remained less explored. In this article, we provide an overview of the contribution of the non-fibrillar components of the extracellular space of the heart to highlight the potential significance of these molecules in fibrosis, with direct evidence for some, although not all of these molecules in their direct contribution to fibrosis. Full article
(This article belongs to the Special Issue Cardiac Fibroblasts and Fibrosis)
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26 pages, 1279 KiB  
Review
Ca2+ Signaling in Cardiac Fibroblasts and Fibrosis-Associated Heart Diseases
by Jianlin Feng, Maria K. Armillei, Albert S. Yu, Bruce T. Liang, Loren W. Runnels and Lixia Yue
J. Cardiovasc. Dev. Dis. 2019, 6(4), 34; https://doi.org/10.3390/jcdd6040034 - 23 Sep 2019
Cited by 41 | Viewed by 7366
Abstract
Cardiac fibrosis is the excessive deposition of extracellular matrix proteins by cardiac fibroblasts and myofibroblasts, and is a hallmark feature of most heart diseases, including arrhythmia, hypertrophy, and heart failure. This maladaptive process occurs in response to a variety of stimuli, including myocardial [...] Read more.
Cardiac fibrosis is the excessive deposition of extracellular matrix proteins by cardiac fibroblasts and myofibroblasts, and is a hallmark feature of most heart diseases, including arrhythmia, hypertrophy, and heart failure. This maladaptive process occurs in response to a variety of stimuli, including myocardial injury, inflammation, and mechanical overload. There are multiple signaling pathways and various cell types that influence the fibrogenesis cascade. Fibroblasts and myofibroblasts are central effectors. Although it is clear that Ca2+ signaling plays a vital role in this pathological process, what contributes to Ca2+ signaling in fibroblasts and myofibroblasts is still not wholly understood, chiefly because of the large and diverse number of receptors, transporters, and ion channels that influence intracellular Ca2+ signaling. Intracellular Ca2+ signals are generated by Ca2+ release from intracellular Ca2+ stores and by Ca2+ entry through a multitude of Ca2+-permeable ion channels in the plasma membrane. Over the past decade, the transient receptor potential (TRP) channels have emerged as one of the most important families of ion channels mediating Ca2+ signaling in cardiac fibroblasts. TRP channels are a superfamily of non-voltage-gated, Ca2+-permeable non-selective cation channels. Their ability to respond to various stimulating cues makes TRP channels effective sensors of the many different pathophysiological events that stimulate cardiac fibrogenesis. This review focuses on the mechanisms of Ca2+ signaling in fibroblast differentiation and fibrosis-associated heart diseases and will highlight recent advances in the understanding of the roles that TRP and other Ca2+-permeable channels play in cardiac fibrosis. Full article
(This article belongs to the Special Issue Cardiac Fibroblasts and Fibrosis)
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17 pages, 922 KiB  
Review
Cardiac Fibroblasts and the Extracellular Matrix in Regenerative and Nonregenerative Hearts
by Luis Hortells, Anne Katrine Z. Johansen and Katherine E. Yutzey
J. Cardiovasc. Dev. Dis. 2019, 6(3), 29; https://doi.org/10.3390/jcdd6030029 - 20 Aug 2019
Cited by 54 | Viewed by 6284
Abstract
During the postnatal period in mammals, the heart undergoes significant remodeling and cardiac cells progressively lose their embryonic characteristics. At the same time, notable changes in the extracellular matrix (ECM) composition occur with a reduction in the components considered facilitators of cellular proliferation, [...] Read more.
During the postnatal period in mammals, the heart undergoes significant remodeling and cardiac cells progressively lose their embryonic characteristics. At the same time, notable changes in the extracellular matrix (ECM) composition occur with a reduction in the components considered facilitators of cellular proliferation, including fibronectin and periostin, and an increase in collagen fiber organization. Not much is known about the postnatal cardiac fibroblast which is responsible for producing the majority of the ECM, but during the days after birth, mammalian hearts can regenerate after injury with only a transient scar formation. This phenomenon has also been described in adult urodeles and teleosts, but relatively little is known about their cardiac fibroblasts or ECM composition. Here, we review the pre-existing knowledge about cardiac fibroblasts and the ECM during the postnatal period in mammals as well as in regenerative environments. Full article
(This article belongs to the Special Issue Cardiac Fibroblasts and Fibrosis)
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10 pages, 252 KiB  
Review
Cardiac Fibroblast to Myofibroblast Phenotype Conversion—An Unexploited Therapeutic Target
by Michael P. Czubryt
J. Cardiovasc. Dev. Dis. 2019, 6(3), 28; https://doi.org/10.3390/jcdd6030028 - 16 Aug 2019
Cited by 32 | Viewed by 4006
Abstract
Fibrosis occurs when the synthesis of extracellular matrix outpaces its degradation, and over time can negatively impact tissue and organ function. In the case of cardiac fibrosis, contraction and relaxation of the heart can be impaired to the point of precipitating heart failure, [...] Read more.
Fibrosis occurs when the synthesis of extracellular matrix outpaces its degradation, and over time can negatively impact tissue and organ function. In the case of cardiac fibrosis, contraction and relaxation of the heart can be impaired to the point of precipitating heart failure, while at the same time fibrosis can result in arrhythmias due to altered electrical properties of the myocardium. The critical event in the evolution of cardiac fibrosis is the phenotype conversion of cardiac fibroblasts to their overly-active counterparts, myofibroblasts: cells demarked by their expression of novel markers such as periostin, by their gain of contractile activity, and by their pronounced and prolonged increase in the production of extracellular matrix components such as collagens. The phenotype change is dramatic, and can be triggered by many stimuli, including mechanical force, inflammatory cytokines, and growth factors. This review will explore fibroblast to myofibroblast transition mechanisms and will consider the therapeutic potential of targeting this process as a means to arrest or even reverse cardiac fibrosis. Full article
(This article belongs to the Special Issue Cardiac Fibroblasts and Fibrosis)
18 pages, 933 KiB  
Review
Cardiac Fibroblast p38 MAPK: A Critical Regulator of Myocardial Remodeling
by Neil A. Turner and Nicola M. Blythe
J. Cardiovasc. Dev. Dis. 2019, 6(3), 27; https://doi.org/10.3390/jcdd6030027 - 7 Aug 2019
Cited by 59 | Viewed by 8257
Abstract
The cardiac fibroblast is a remarkably versatile cell type that coordinates inflammatory, fibrotic and hypertrophic responses in the heart through a complex array of intracellular and intercellular signaling mechanisms. One important signaling node that has been identified involves p38 MAPK; a family of [...] Read more.
The cardiac fibroblast is a remarkably versatile cell type that coordinates inflammatory, fibrotic and hypertrophic responses in the heart through a complex array of intracellular and intercellular signaling mechanisms. One important signaling node that has been identified involves p38 MAPK; a family of kinases activated in response to stress and inflammatory stimuli that modulates multiple aspects of cardiac fibroblast function, including inflammatory responses, myofibroblast differentiation, extracellular matrix turnover and the paracrine induction of cardiomyocyte hypertrophy. This review explores the emerging importance of the p38 MAPK pathway in cardiac fibroblasts, describes the molecular mechanisms by which it regulates the expression of key genes, and highlights its potential as a therapeutic target for reducing adverse myocardial remodeling. Full article
(This article belongs to the Special Issue Cardiac Fibroblasts and Fibrosis)
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