The living scar - cardiac fibroblasts and the injured heart
File(s)
Accepted version
Author(s)
Rog-Zielinska, EA
Norris, RA
Kohl, P
Markwald, R
Type
Journal Article
Abstract
Cardiac scars, often dubbed ‘dead tissue’, are very much alive, with heterocellular activity contributing to the maintenance of structural and mechanical integrity following heart injury. To form a scar, non-myocytes such as fibroblasts are recruited from intra- and extra-cardiac sources. Fibroblasts perform important autocrine and paracrine signaling functions. They also establish mechanical and, as is increasingly evident, electrical junctions with other cells. While fibroblasts were previously thought to act simply as electrical insulators, they may be electrically connected among themselves and, under some circumstances, to other cells including cardiomyocytes. A better understanding of these biophysical interactions will help to target scar structure and function, and will facilitate the development of novel therapies aimed at modifying scar properties for patient benefit.
Date Issued
2016-01-14
Date Acceptance
2016-01-01
Citation
Trends in Molecular Medicine, 2016, 22 (2), pp.99-114
ISSN
1471-4914
Publisher
Elsevier
Start Page
99
End Page
114
Journal / Book Title
Trends in Molecular Medicine
Volume
22
Issue
2
Copyright Statement
© 2016, Elsevier Ltd. All rights reserved. This manuscript is licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International http://creativecommons.org/licenses/by-nc-nd/4.0/
Sponsor
British Heart Foundation
Identifier
http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:000370091000004&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=1ba7043ffcc86c417c072aa74d649202
Grant Number
FS/12/17/29532
Subjects
Science & Technology
Life Sciences & Biomedicine
Biochemistry & Molecular Biology
Cell Biology
Medicine, Research & Experimental
Research & Experimental Medicine
MARROW-DERIVED CELLS
MYOCARDIAL INFARCT REPAIR
INTERSTITIAL LUNG-DISEASE
GAP-JUNCTION CHANNELS
IN-VIVO
VENTRICULAR-TACHYCARDIA
GROWTH-FACTOR
ATRIAL-FIBRILLATION
MEMBRANE NANOTUBES
CHEMOATTRACTANT PROTEIN-1
cardiac
fibrosis
non-myocyte
Autocrine Communication
Cell Movement
Chemokine CCL2
Chemokine CXCL10
Cicatrix
Fibroblasts
Gap Junctions
Gene Expression Regulation
Heart Injuries
Humans
MicroRNAs
Myocytes, Cardiac
Paracrine Communication
Signal Transduction
Transforming Growth Factor beta
Immunology
06 Biological Sciences
11 Medical And Health Sciences
Publication Status
Published