Cardiac Ablation of SOCS3 Aggravates DOCA-Salt-Induced Hypertrophic Remodeling by Activation of Gp130-Dependent Signaling in Mice
Author(s) -
Shuang Liu,
Lixin Liu,
YunLong Zhang,
Song Lai,
Yunpeng Xie,
Nannan Li,
Hongxia Wang,
Yunlong Xia,
Ying Liu,
HuiHua Li
Publication year - 2018
Publication title -
cellular physiology and biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.486
H-Index - 87
eISSN - 1421-9778
pISSN - 1015-8987
DOI - 10.1159/000489757
Subject(s) - socs3 , endocrinology , cardiac fibrosis , medicine , fibrosis , glycoprotein 130 , ventricular remodeling , inflammation , heart failure , eplerenone , mineralocorticoid receptor , receptor , interleukin 6 , cancer , suppressor
Cardiac remodeling is a critical pathogenetic process leading to heart failure. Suppressor of cytokine signaling-3 (SOCS3) is demonstrated as a key negative regulator of the gp130 receptor to inhibit cardiac hypertrophy. However, the role of SOCS3 in deoxycorticosterone-acetate (DOCA)-salt-induced cardiac remodeling remains unclear.
Accelerating Research
Robert Robinson Avenue,
Oxford Science Park, Oxford
OX4 4GP, United Kingdom
Address
John Eccles HouseRobert Robinson Avenue,
Oxford Science Park, Oxford
OX4 4GP, United Kingdom