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Myocyte contractility with caspase inhibition and simulated hyperkalemic cardioplegic arrest.
Pharmacologic inhibition of intracellular caspases after myocardial infarction attenuates left ventricular remodeling: a potentially novel pathway.
Caspase inhibition attenuates contractile dysfunction following cardioplegic arrest and rewarming in the setting of left ventricular failure.
Calpain inhibition preserves myocardial structure and function following myocardial infarction.
Caspase inhibition modulates left ventricular remodeling following myocardial infarction through cellular and extracellular mechanisms.