Key result
Genetic deletion or pharmacological inhibition of Gasdermin D attenuated myocardial injury, reduced infarct size, and significantly improved post-AMI survival (78.7% vs 50%) in mice.
Why the study?
Acute myocardial infarction induces blood leukocytosis correlating inversely with survival, but the molecular mechanisms driving leukocytosis in the infarcted heart remain poorly understood.
Does GSDMD inhibition reduce infarct size and improve cardiac function and survival in acute myocardial infarction?
Population
Mouse model of acute myocardial infarction
Comparison
GSDMD knockout or pharmacological inhibition vs controls
Design
Preclinical animal and mechanistic study
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GSDMD targeting shows preclinical promise in AMI; leaves open whether inhibition improves human survival or ejection fraction.
Does GSDMD inhibition reduce infarct size and improve cardiac function and survival in acute myocardial infarction?
Absolute Event Rate: 78.7% vs 50%
p-value: p=0.0108
Inhibition of GSDMD reduces early neutrophil mobilization and infarct size, presenting a potential novel therapeutic target for preventing post-AMI heart failure.
A 2021 study studied Acute myocardial infarction (n=234). Gasdermin D (GSDMD) inhibition (genetic deletion or necrosulfonamide) vs. Wild-type or vehicle control was evaluated on Post-AMI survival (murine model) (p=0.0108). Genetic deletion or pharmacological inhibition of Gasdermin D attenuated myocardial injury, reduced infarct size, and significantly improved post-AMI survival (78.7% vs 50%) in mice.