Signaling Pathways in Organ Fibrosis

A special issue of Journal of Clinical Medicine (ISSN 2077-0383).

Deadline for manuscript submissions: closed (31 March 2017)

Special Issue Editors


E-Mail Website
Guest Editor
1. Department of Internal Medicine and Cardiology, Charité University Medicine Berlin, Campus Virchow Klinikum (CVK), Berlin, Germany
2. Berlin Center for Regenerative Therapies (BCRT), Berlin, Germany
Interests: inflammatory cardiomyopathy; diabetic cardiopathy; ischemic cardiopathy; diastolic dysfunction; endothelial dysfunction; peptide systems; experimental and clinical studies in cardiology; stem cells

E-Mail
Guest Editor
Berlin-Brandenburg Center for Regenerative Therapies (BCRT), Berlin, Germany
Interests: diabetic cardiopathy; endothelial dysfunction; cardiac regeneration; mesenchymal stem cells; high-density lipoprotein

Special Issue Information

Dear Colleagues,

Fibroblasts, traditionally recognized as sentinel cells important for the architecture of the extracellular matrix, are more and more appreciated for their role in inflammation, angiogenesis, and electrophysiology. Particularly, their function as an inflammatory supporter cell, provoking chronic inflammation upon aberrant activation is gaining more attention in several fields, ranging from cardiology to pulmonology, nephrology, cancer, and autoimmune diseases. Fibroblasts differ from the anatomical site, the disease status, and even within the same tissue, and may have distinct cellular origins. Fibrosis, as such, is a complex dynamic process involving several cellular interactions and several signaling pathways. Further understanding of particularly the reciprocal link between inflammation and fibrosis is vital for establishing novel treatment strategies for diseases with fibrosis and inflammation.

Please join us in presenting this Special Issue on the state-of-the-art research currently being performed on organ fibrosis in different disciplines to gather our knowledge in view of gaining further common insights in this complex process.

Prof. Dr. med. Carsten Tschöpe
Dr. Sophie Van Linthout
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. Journal of Clinical Medicine 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 2600 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
  • myofibroblasts
  • crosslinking
  • TGF-β
  • tenascin-C
  • lysyloxidases
  • galectin-3
  • remodeling
  • stroma
  • fibrocytes
  • endothelial-to-mesenchymal-transition

Published Papers (1 paper)

Order results
Result details
Select all
Export citation of selected articles as:

Review

2245 KiB  
Review
The Soft- and Hard-Heartedness of Cardiac Fibroblasts: Mechanotransduction Signaling Pathways in Fibrosis of the Heart
by Kate M. Herum, Ida G. Lunde, Andrew D. McCulloch and Geir Christensen
J. Clin. Med. 2017, 6(5), 53; https://doi.org/10.3390/jcm6050053 - 19 May 2017
Cited by 125 | Viewed by 22962
Abstract
Cardiac fibrosis, the excessive accumulation of extracellular matrix (ECM), remains an unresolved problem in most forms of heart disease. In order to be successful in preventing, attenuating or reversing cardiac fibrosis, it is essential to understand the processes leading to ECM production and [...] Read more.
Cardiac fibrosis, the excessive accumulation of extracellular matrix (ECM), remains an unresolved problem in most forms of heart disease. In order to be successful in preventing, attenuating or reversing cardiac fibrosis, it is essential to understand the processes leading to ECM production and accumulation. Cardiac fibroblasts are the main producers of cardiac ECM, and harbor great phenotypic plasticity. They are activated by the disease-associated changes in mechanical properties of the heart, including stretch and increased tissue stiffness. Despite much remaining unknown, an interesting body of evidence exists on how mechanical forces are translated into transcriptional responses important for determination of fibroblast phenotype and production of ECM constituents. Such mechanotransduction can occur at multiple cellular locations including the plasma membrane, cytoskeleton and nucleus. Moreover, the ECM functions as a reservoir of pro-fibrotic signaling molecules that can be released upon mechanical stress. We here review the current status of knowledge of mechanotransduction signaling pathways in cardiac fibroblasts that culminate in pro-fibrotic gene expression. Full article
(This article belongs to the Special Issue Signaling Pathways in Organ Fibrosis)
Show Figures

Graphical abstract

Back to TopTop