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          Institute: MPI für Herz- und Lungenforschung (W. G. Kerckhoff Institut)     Collection: Yearbook_2015     Display Documents

ID: 711875.0, MPI für Herz- und Lungenforschung (W. G. Kerckhoff Institut) / Yearbook_2015
Therapeutic targeting of the oncostatin M receptor-beta prevents inflammatory heart failure
Authors:Poling, J.; Gajawada, P.; Richter, M.; Lorchner, H.; Polyakova, V.; Kostin, S.; Shin, J.; Boettger, T.; Walther, T.; Rees, W.; Wietelmann, A.; Warnecke, H.; Kubin, T.; Braun, T.
Date of Publication (YYYY-MM-DD):2014-01
Title of Journal:Basic Res Cardiol
Issue / Number:1
Start Page:396
Audience:Not Specified
Abstract / Description:Heart failure (HF) is a common and potentially deadly condition, which frequently develops as a consequence of various diseases of the heart. The incidence of heart failure continuously increases in aging societies illustrating the need for new therapeutic approaches. We recently discovered that continuous activation of oncostatin M (OSM), a cytokine of the interleukin-6 family that induces dedifferentiation of cardiomyocytes, promotes progression of heart failure in dilative cardiomyopathy. To evaluate whether inhibition of OSM signaling represents a meaningful therapeutic approach to prevent heart failure we attenuated OSM-receptor (Obeta) signaling in a mouse model of inflammatory dilative cardiomyopathy. We found that administration of an antibody directed against the extracellular domain of Obeta or genetic inactivation of a single allele of the Obeta gene reduced cardiomyocyte remodeling and dedifferentiation resulting in improved cardiac performance and increased survival. We conclude that pharmacological attenuation of long-lasting Obeta signaling is a promising strategy to treat different types and stages of HF that go along with infiltration by OSM-releasing inflammatory cells.
External Publication Status:published
Document Type:Article
Communicated by:MPI für Herz- und Lungenforschung
Affiliations:MPI für physiologische und klinische Forschung
External Affiliations:%^ 1435822261
Identifiers:ISSN:1435-1803 (Electronic) 0300-8428 (Linking) %R 10.1007/s00395-013-0396-3
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