Document Detail


SOCS3: A novel therapeutic target for cardioprotection.
MedLine Citation:
PMID:  24058778     Owner:  NLM     Status:  PubMed-not-MEDLINE    
Abstract/OtherAbstract:
The suppressors of cytokine signaling (SOCS) family of proteins are cytokine-inducible inhibitors of Janus kinase (JAK)-signal transducer and activator of the transcription (STAT) signaling pathways. Among the family, SOCS1 and SOCS3 potently suppress cytokine actions by inhibiting JAK kinase activities. The generation of mice lacking individual SOCS genes has been instrumental in defining the role of individual SOCS proteins in specific cytokine pathways in vivo; SOCS1 is an essential negative regulator of interferon-γ (IFNγ) and SOCS3 is an essential negative regulator of leukemia inhibitory factor (LIF). JAK-STAT3 activating cytokines have exhibited cardioprotective roles in the heart. The cardiac-specific deletion of SOCS3 enhances the activation of cardioprotective signaling pathways, inhibits myocardial apoptosis and fibrosis and results in the inhibition of left ventricular remodeling after myocardial infarction (MI). We propose that myocardial SOCS3 is a key determinant of left ventricular remodeling after MI, and SOCS3 may serve as a novel therapeutic target to prevent left ventricular remodeling after MI. In this review, we discuss the signaling pathways mediated by JAK-STAT and SOCS proteins and their roles in the development of myocardial injury under stress (e.g., pressure overload, viral infection and ischemia).
Authors:
Hideo Yasukawa; Takanobu Nagata; Toyoharu Oba; Tsutomu Imaizumi
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Publication Detail:
Type:  Journal Article; Review    
Journal Detail:
Title:  JAK-STAT     Volume:  1     ISSN:  2162-3988     ISO Abbreviation:  JAKSTAT     Publication Date:  2012 Oct 
Date Detail:
Created Date:  2013-09-23     Completed Date:  2014-06-24     Revised Date:  2014-06-24    
Medline Journal Info:
Nlm Unique ID:  101591376     Medline TA:  JAKSTAT     Country:  United States    
Other Details:
Languages:  eng     Pagination:  234-40     Citation Subset:  -    
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