Key result
In a mouse model of myocardial infarction, continuous gp130-mediated STAT3 activation resulted in higher mortality, increased left ventricular rupture, and sustained cardiac inflammation.
Impaired downregulation of gp130-mediated STAT3 activation promotes adverse remodeling, inflammation, and heart failure in subacute myocardial infarction.
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May caution against sustained STAT3 activation post-MI; leaves open optimal modulation timing in translational models.
Hilfiker‐Kleiner et al. (2010) studied Myocardial infarction. Cardiomyocyte-specific gp130 Y757F mutation vs. Nonmutant littermates was evaluated on Mortality, left ventricular rupture, and cardiac inflammation. In a mouse model of myocardial infarction, continuous gp130-mediated STAT3 activation resulted in higher mortality, increased left ventricular rupture, and sustained cardiac inflammation.
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