Ablation of SOCS3 in Cardiomyocytes Exacerbates Cardiac hypertrophy and Dysfunction by Increasing GRP78-medieated ER Stress after pressure overload
Ontology highlight
ABSTRACT:
INSTRUMENT(S): Q Exactive Plus
ORGANISM(S): Mus Musculus (mouse)
SUBMITTER: 
Shuang Liu
LAB HEAD: Huihua Li
PROVIDER: PXD014946 | Pride | 2021-09-08
REPOSITORIES: Pride
Dataset's files
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Publications
SOCS3 Negatively Regulates Cardiac Hypertrophy via Targeting GRP78-Mediated ER Stress During Pressure Overload.
Liu Shuang S Sun Wen-Chang WC Zhang Yun-Long YL Lin Qiu-Yue QY Liao Jia-Wei JW Song Gui-Rong GR Ma Xiao-Lei XL Li Hui-Hua HH Zhang Bo B
Frontiers in cell and developmental biology 20210126
Pressure overload-induced hypertrophic remodeling is a critical pathological process leading to heart failure (HF). Suppressor of cytokine signaling-3 (SOCS3) has been demonstrated to protect against cardiac hypertrophy and dysfunction, but its mechanisms are largely unknown. Using primary cardiomyocytes and cardiac-specific SOCS3 knockout (SOCS3cko) or overexpression mice, we demonstrated that modulation of SOCS3 level influenced cardiomyocyte hypertrophy, apoptosis and cardiac dysfunction indu ...[more]
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