Key result
Elamipretide preserves coronary endothelial mitochondria and reduces vascular injury in a porcine metabolic syndrome model.
Why the study?
Metabolic syndrome leads to cardiac vascular injury involving endothelial cell mitochondrial dysfunction, but the effects of chronic mitoprotection on coronary vascular injury and dysfunction are unclear.
Does elamipretide attenuate coronary vascular injury and dysfunction in a porcine model of metabolic syndrome?
Comparison
Elamipretide treatment vs untreated metabolic syndrome and lean controls
Design
Preclinical study with in vivo and ex vivo assessments
Follow-up
16 weeks (4 weeks of treatment)
Authors
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Mitoprotection may attenuate coronary vascular injury in experimental MetS; leaves open translation to human patients and need for clinical trials.
Does elamipretide attenuate coronary vascular injury and dysfunction in a porcine model of metabolic syndrome?
Chronic mitoprotection with elamipretide preserves coronary endothelial cell mitochondria and attenuates vascular injury in a porcine model of metabolic syndrome, though it does not fully restore myocardial perfusion.
Yuan et al. (2017) studied Metabolic syndrome (n=18). Elamipretide vs. Untreated metabolic syndrome and lean controls was evaluated on Coronary endothelial cell mitochondrial density, apoptosis, oxidative stress, myocardial microvascular density, and coronary endothelial function. Elamipretide preserved coronary endothelial cell mitochondria and decreased vascular injury and subendocardial microvascular loss in a porcine model of metabolic syndrome.
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