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SOCS1 gene transfer accelerates the transition to heart failure through the inhibition of the gp130/JAK/STAT pathway
Author(s) -
Antonio Cittadini,
M. Monti,
Guido Iaccarino,
Maria Carmina Castiello,
Alfonso Baldi,
Eduardo Bossone,
Salvatore Longobardi,
Alberto M. Marra,
Valentina Petrillo,
Lavinia Saldamarco,
Matthew J. During,
Luigi Saccà,
Gianluigi Condorelli
Publication year - 2012
Publication title -
cardiovascular research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.774
H-Index - 219
eISSN - 1755-3245
pISSN - 0008-6363
DOI - 10.1093/cvr/cvs261
Subject(s) - suppressor of cytokine signaling 1 , pressure overload , glycoprotein 130 , jak stat signaling pathway , heart failure , socs3 , medicine , muscle hypertrophy , cytokine , endocrinology , biology , janus kinase , stat3 , signal transduction , interleukin 6 , microbiology and biotechnology , receptor , tyrosine kinase , cardiac hypertrophy , cancer , suppressor
The suppressors of cytokine signalling (SOCS) are identified inhibitors of cytokine and growth factor signalling that act via the Janus kinase (JAK) signal transducers and activators of transcription (STAT) pathways. Aberrant JAK/STAT signalling promotes progression from hypertrophy to heart failure. Little information is available concerning the role of SOCS in the transition from hypertrophy to heart failure. To this aim, we investigated the effects of SOCS1 overexpression obtained by in vivo adeno-associated gene transfer using an aortopulmonary cross-clamping technique in a chronic pressure-overload cardiac rat model.

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