Why the study?
Myocardial infarction is a common cardiovascular disease with high morbidity and mortality, prompting investigation into the role of IFIT3 in MI.
Does lentivirus-mediated RNA interference of IFIT3 expression reduce inflammatory response and myocardial fibrosis in mice with myocardial infarction?
Population
Mice with MI induced by LAD coronary artery ligation
Comparison
Lentivirus-mediated RNA interference of IFIT3 vs control
Design
Preclinical animal study
Follow-up
4 weeks
Authors
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Does not support IFIT3 targeting in clinical MI care; leaves open therapeutic translation from rodent models.
Does lentivirus-mediated RNA interference of IFIT3 expression reduce inflammatory response and myocardial fibrosis in mice with myocardial infarction?
Knockdown of IFIT3 protects against myocardial injury, inflammation, and fibrosis following myocardial infarction in a mouse model, potentially by blocking the MAPK pathway.
Sun et al. (2021) studied this question.
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