title: The Living Scar--Cardiac Fibroblasts and the Injured Heart.
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.
authors.affiliation: Institute for Experimental Cardiovascular Medicine, University of Freiburg, Freiburg, Germany; National Heart and Lung Institute, Imperial College London, London, UK.
authors.forename: Eva A
authors.initials: EA
authors.lastname: Rog-Zielinska
authors.affiliation: Department of Regenerative Medicine and Cell Biology, Medical University of South Carolina, Charleston, SC, USA.
authors.forename: Russell A
authors.initials: RA
authors.lastname: Norris
authors.affiliation: Institute for Experimental Cardiovascular Medicine, University of Freiburg, Freiburg, Germany; National Heart and Lung Institute, Imperial College London, London, UK. Electronic address: peter.kohl@universitaets-herzzentrum.de.
authors.forename: Peter
authors.initials: P
authors.lastname: Kohl
authors.affiliation: Department of Regenerative Medicine and Cell Biology, Medical University of South Carolina, Charleston, SC, USA.
authors.forename: Roger
authors.initials: R
authors.lastname: Markwald
mesh_terms: D019898:Autocrine Communication; D002465:Cell Movement; D018932:Chemokine CCL2 / Q000235:genetics / Q000378:metabolism; D054357:Chemokine CXCL10 / Q000235:genetics / Q000378:metabolism; D002921:Cicatrix / Q000235:genetics / Q000378:metabolism* / Q000473:pathology; D005347:Fibroblasts / Q000378:metabolism* / Q000473:pathology; D017629:Gap Junctions / Q000378:metabolism* / Q000648:ultrastructure; D005786:Gene Expression Regulation; D006335:Heart Injuries / Q000235:genetics / Q000378:metabolism* / Q000473:pathology; D006801:Humans; D035683:MicroRNAs / Q000235:genetics / Q000378:metabolism; D032383:Myocytes, Cardiac / Q000378:metabolism* / Q000473:pathology; D019899:Paracrine Communication; D015398:Signal Transduction; D016212:Transforming Growth Factor beta / Q000235:genetics / Q000378:metabolism
chemical_list: C111835:CCL2 protein, human; C114753:CXCL10 protein, human; D018932:Chemokine CCL2; D054357:Chemokine CXCL10; D035683:MicroRNAs; D016212:Transforming Growth Factor beta
keywords: cardiac; fibrosis; non-myocyte