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Special Issue "Role of Stromal Cell Population in Myocardial Remodelling"

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Biochemistry".

Deadline for manuscript submissions: 31 May 2021.

Special Issue Editors

Dr. Gabriela Kania
Website
Guest Editor
Center of Experimental Rheumatology, Department of Rheumatology, University Hospital Zurich, Wagistrasse 14, 8952 Schlieren, Switzerland
Interests: mechanism of multiorgan remodeling; heart pathogenesis; fibrosis; fibroblast; arrhythmia; conduction system; 3D cardiac models; systemic sclerosis; heart dysfunction
Special Issues and Collections in MDPI journals
Dr. Przemyslaw Blyszczuk
Website
Guest Editor
Center of Experimental Rheumatology, Department of Rheumatology, University Hospital Zurich, Wagistrasse 14, 8952 Schlieren, Switzerland
Interests: myocarditis; inflammatory dilated cardiomyopathy; innate and adaptive immunity; mouse models of heart failure; myocardial inflammation; Wnt signaling

Special Issue Information

Dear Colleagues,

Stromal cells represent a heterogeneous cell population with connective tissue characteristics, displaying diverse differentiation potentials depending on the tissue and organ localization and playing a specific role in tissue homeostasis and remodeling. Cardiac stromal cells create the appropriate architecture for cardiomyocytes that ensures suitable cardiomyocyte alignment and function in homeostasis. During myocardial remodeling, stromal cells contribute to inflammatory and pro-fibrotic responses closely cross-talking with inflammatory and endothelial cells, indicating stromal cell populations as key objectives in targeted therapies. Nevertheless, the precise role of distinct cardiac stromal cell populations still remains not completely understood. Therefore, in this Special Issue, we encourage submission of manuscripts describing the subpopulations of cardiac stromal cells, their characteristic, function and role in homeostasis and remodeling mainly in cardiovascular and rheumatic diseases in in vitro or ex vivo setups including 3D culture models and in vivo models. We are highly interested in manuscripts reporting application of preclinical and clinical strategies targeting stromal cell activation or function. Likewise, studies on the specific signaling pathways responsible for activation and differentiation of cardiac stromal cells in these diseases and manuscripts describing cardiac immune cell–stromal cell cross-talk are within the scope of this Special Issue. 

Dr. Przemyslaw Blyszczuk
Dr. Gabriela Kania
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 papers will be 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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

  • Stromal cells, fibroblasts
  • Heart failure in rheumatic diseases
  • Cardiovascular diseases
  • Myocardial inflammation
  • Myocardial fibrosis
  • Myocardial remodeling
  • Animal models of heart failure
  • 3D cardiac models

Published Papers (2 papers)

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Research

Open AccessArticle
Selective Cardiomyocyte Oxidative Stress Leads to Bystander Senescence of Cardiac Stromal Cells
Int. J. Mol. Sci. 2021, 22(5), 2245; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22052245 - 24 Feb 2021
Abstract
Accumulation of senescent cells in tissues during normal or accelerated aging has been shown to be detrimental and to favor the outcomes of age-related diseases such as heart failure (HF). We have previously shown that oxidative stress dependent on monoamine oxidase A (MAOA) [...] Read more.
Accumulation of senescent cells in tissues during normal or accelerated aging has been shown to be detrimental and to favor the outcomes of age-related diseases such as heart failure (HF). We have previously shown that oxidative stress dependent on monoamine oxidase A (MAOA) activity in cardiomyocytes promotes mitochondrial damage, the formation of telomere-associated foci, senescence markers, and triggers systolic cardiac dysfunction in a model of transgenic mice overexpressing MAOA in cardiomyocytes (Tg MAOA). However, the impact of cardiomyocyte oxidative stress on the cardiac microenvironment in vivo is still unclear. Our results showed that systolic cardiac dysfunction in Tg MAOA mice was strongly correlated with oxidative stress induced premature senescence of cardiac stromal cells favoring the recruitment of CCR2+ monocytes and the installation of cardiac inflammation. Understanding the interplay between oxidative stress induced premature senescence and accelerated cardiac dysfunction will help to define new molecular pathways at the crossroad between cardiac dysfunction and accelerated aging, which could contribute to the increased susceptibility of the elderly to HF. Full article
(This article belongs to the Special Issue Role of Stromal Cell Population in Myocardial Remodelling)
Open AccessArticle
The AP-1 Transcription Factor Fosl-2 Regulates Autophagy in Cardiac Fibroblasts during Myocardial Fibrogenesis
Int. J. Mol. Sci. 2021, 22(4), 1861; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22041861 - 13 Feb 2021
Abstract
Background: Pathological activation of cardiac fibroblasts is a key step in development and progression of cardiac fibrosis and heart failure. This process has been associated with enhanced autophagocytosis, but molecular mechanisms remain largely unknown. Methods and Results: Immunohistochemical analysis of endomyocardial biopsies showed [...] Read more.
Background: Pathological activation of cardiac fibroblasts is a key step in development and progression of cardiac fibrosis and heart failure. This process has been associated with enhanced autophagocytosis, but molecular mechanisms remain largely unknown. Methods and Results: Immunohistochemical analysis of endomyocardial biopsies showed increased activation of autophagy in fibrotic hearts of patients with inflammatory cardiomyopathy. In vitro experiments using mouse and human cardiac fibroblasts confirmed that blockade of autophagy with Bafilomycin A1 inhibited fibroblast-to-myofibroblast transition induced by transforming growth factor (TGF)-β. Next, we observed that cardiac fibroblasts obtained from mice overexpressing transcription factor Fos-related antigen 2 (Fosl-2tg) expressed elevated protein levels of autophagy markers: the lipid modified form of microtubule-associated protein 1A/1B-light chain 3B (LC3BII), Beclin-1 and autophagy related 5 (Atg5). In complementary experiments, silencing of Fosl-2 with antisense GapmeR oligonucleotides suppressed production of type I collagen, myofibroblast marker alpha smooth muscle actin and autophagy marker Beclin-1 in cardiac fibroblasts. On the other hand, silencing of either LC3B or Beclin-1 reduced Fosl-2 levels in TGF-β-activated, but not in unstimulated cells. Using a cardiac hypertrophy model induced by continuous infusion of angiotensin II with osmotic minipumps, we confirmed that mice lacking either Fosl-2 (Ccl19CreFosl2flox/flox) or Atg5 (Ccl19CreAtg5flox/flox) in stromal cells were protected from cardiac fibrosis. Conclusion: Our findings demonstrate that Fosl-2 regulates autophagocytosis and the TGF-β-Fosl-2-autophagy axis controls differentiation of cardiac fibroblasts. These data provide a new insight for the development of pharmaceutical targets in cardiac fibrosis. Full article
(This article belongs to the Special Issue Role of Stromal Cell Population in Myocardial Remodelling)
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