Dataset Information
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
Publications
SOCS3 Negatively Regulates Cardiac Hypertrophy via Targeting GRP78-Mediated ER Stress During Pressure Overload.
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]
