Why the study?
Cardiac glucose metabolism is critically involved in the pathophysiology of myocardial infarction, but whether Qiliqiangxin improves myocardial glucose uptake and aerobic oxidation after MI remained to be investigated.
Does Qiliqiangxin improve myocardial glucose uptake and aerobic oxidation in a murine model of post-MI heart failure?
Population
Murine model of post-MI heart failure
Comparison
Qiliqiangxin treatment with or without HIF-1α-shRNA transduction
Design
Preclinical animal study
Authors
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May improve post-MI HF via HIF-1α in mice; leaves open human translation.
Does Qiliqiangxin improve myocardial glucose uptake and aerobic oxidation in a murine model of post-MI heart failure?
Qiliqiangxin improves cardiac glucose metabolism and left ventricular ejection fraction in post-MI heart failure via the HIF-1α/MIF/AMPK signaling axis in a murine model.
Wang et al. (2026) studied this question.
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