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          Institute: MPI für Herz- und Lungenforschung (W. G. Kerckhoff Institut)     Collection: Yearbook 2016     Display Documents



ID: 724009.0, MPI für Herz- und Lungenforschung (W. G. Kerckhoff Institut) / Yearbook 2016
Myostatin induces interstitial fibrosis in the heart via TAK1 and p38
Authors:Biesemann, N.; Mendler, L.; Kostin, S.; Wietelmann, A.; Borchardt, T.; Braun, T.
Date of Publication (YYYY-MM-DD):2015-09
Title of Journal:Cell Tissue Res
Volume:361
Issue / Number:3
Start Page:779
End Page:787
Audience:Not Specified
Abstract / Description:Myostatin, a member of the TGF-beta superfamily of secreted growth factors, is a negative regulator of skeletal muscle growth. In the heart, it is expressed at lower levels compared to skeletal muscle but up-regulated under disease conditions. Cre recombinase-mediated inactivation of myostatin in adult cardiomyocytes leads to heart failure and increased mortality but cardiac function of surviving mice is restored after several weeks probably due to compensatory expression in non-cardiomyocytes. To study long-term effects of increased myostatin expression in the heart and to analyze the putative crosstalk between cardiomyocytes and fibroblasts, we overexpressed myostatin in cardiomyocytes. Increased expression of myostatin in heart muscle cells caused interstitial fibrosis via activation of the TAK-1-MKK3/6-p38 signaling pathway, compromising cardiac function in older mice. Our results uncover a novel role of myostatin in the heart and highlight the necessity for tight regulation of myostatin to maintain normal heart function.
External Publication Status:published
Document Type:Article
Communicated by:n.n.
Affiliations:MPI für physiologische und klinische Forschung
Identifiers:ISSN:1432-0878 (Electronic) 0302-766X (Linking) %R 10.1007/s00441-015-2139-2
URL:http://www.ncbi.nlm.nih.gov/pubmed/25725788
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