Trimetazidine: Activating AMPK Signal to Ameliorate Coronary Microcirculation Dysfunction after Myocardial Infarction
Why the study?
Although trimetazidine protects against myocardial ischemia-reperfusion injury, its role in ischemia-reperfusion-induced endothelial cell dysfunction and coronary microcirculation improvement remained to be investigated.
Population
Myocardial I/R mouse model and in vitro endothelial cell OGD/R model
Comparison
Trimetazidine vs control, with and without compound C
Design
Preclinical animal and in vitro mechanistic study
Authors
Discussion
Loading...
Member takes
Implication
Supports trimetazidine for I/R microvascular injury in models; leaves open clinical translation and human trials.
Structured PICO
P
Population
Myocardial ischemia-reperfusion (I/R) mouse model and in vitro oxygen-glucose deprivation/reperfusion (OGD/R) model in endothelial cells
I
Intervention
Trimetazidine administered for 7 days before myocardial I/R model establishment
C
Comparator
Untreated myocardial I/R and OGD/R models
O
Outcome
Myocardial injury, microvascular function, and barrier injurysurrogate
Trimetazidine ameliorates myocardial ischemia-reperfusion-induced coronary microcirculation dysfunction by activating AMPK signaling in preclinical models.
Cite This Study
Qu et al. (2025) studied this question.