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Oncostatin m is a major mediator of cardiomyocyte dedifferentiation and remodeling.
MedLine Citation:
PMID:  22056139     Owner:  NLM     Status:  In-Data-Review    
Abstract/OtherAbstract:
Cardiomyocyte remodeling, which includes partial dedifferentiation of cardiomyocytes, is a process that occurs during both acute and chronic disease processes. Here, we demonstrate that oncostatin M (OSM) is a major mediator of cardiomyocyte dedifferentiation and remodeling during acute myocardial infarction (MI) and in chronic dilated cardiomyopathy (DCM). Patients suffering from DCM show a strong and lasting increase of OSM expression and signaling. OSM treatment induces dedifferentiation of cardiomyocytes and upregulation of stem cell markers and improves cardiac function after MI. Conversely, inhibition of OSM signaling suppresses cardiomyocyte remodeling after MI and in a mouse model of DCM, resulting in deterioration of heart function after MI but improvement of cardiac performance in DCM. We postulate that dedifferentiation of cardiomyocytes initially protects stressed hearts but fails to support cardiac structure and function upon continued activation. Manipulation of OSM signaling provides a means to control the differentiation state of cardiomyocytes and cellular plasticity.
Authors:
Thomas Kubin; Jochen Pöling; Sawa Kostin; Praveen Gajawada; Stefan Hein; Wolfgang Rees; Astrid Wietelmann; Minoru Tanaka; Holger Lörchner; Silvia Schimanski; Marten Szibor; Henning Warnecke; Thomas Braun
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Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  Cell stem cell     Volume:  9     ISSN:  1875-9777     ISO Abbreviation:  Cell Stem Cell     Publication Date:  2011 Nov 
Date Detail:
Created Date:  2011-11-07     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  101311472     Medline TA:  Cell Stem Cell     Country:  United States    
Other Details:
Languages:  eng     Pagination:  420-32     Citation Subset:  IM    
Copyright Information:
Copyright © 2011 Elsevier Inc. All rights reserved.
Affiliation:
Department of Cardiac Development and Remodelling, Max Planck Institute for Heart and Lung Research, Ludwigstrasse 43, Bad Nauheim, 61321, Germany.
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