Table 1. Key genetic mouse models supporting a role for STAT3 in cardiac ischemia-reperfusion and heart failure.

Ischemia-reperfusion	• Ischemic pre/post-conditioning lost in TNFα knockout,1 TNFα receptor knockout,2 IL-6 knockout3 or cardiac-myocyte STAT3 knockout mice4 • Cardiac myocyte STAT3-deficient mice show enhanced sensitivity to ischemia-reperfusion injury5
Heart failure	• Cardiac myocyte STAT3-deficient mice show reduced myocardial capillary density and increased interstitial fibrosis within 4 mo, followed by dilated cardiomyopathy with impaired cardiac function and premature death due to heart failure5
	• Cardiac myocyte-targeted STAT3 knockout mice show greater sensitivity to inflammation, cardiac fibrosis and heart failure with advanced age6
	• Cardiac myocyte-specific gp130 knockout mice develop heart failure in response to pressure overload accompanied by increased cardiac myocyte apoptosis7
	• Mice with reduced STAT3 activity/levels have increased susceptibility to doxorubicin-induced heart failure and greater susceptibility to LPS-induced toxicity8
	• Mice with cardiac myocyte-targeted STAT3 overexpression develop cardiac hypertrophy but are resistant to doxorubicin-induced cardiomyopathy9