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A working model of SOCS3-mediated cardioprotection in pressure overloaded mice. Pressure overload induces reduction of SOCS3 in cardiomyocytes, which in turn reduces GRP78 degradation by the proteasome and causes activation of ER stress and mitophagy, thereby leading to cardiac hypertrophy and dysfunction. Conversely, these effects are attenuated by overexpression of SOCS3.
