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Study wrapper · #598

Hexarelin treatment preserves myocardial function and reduces cardiac fibrosis in a mouse model of acute myocardial infarction.

McDonald H, Peart J, Kurniawan N, et al. Physiological reports. 2018.
Weak / noneAnimal (in vivo)Mentions: Hexarelin

Editor's note

In a mouse model of myocardial infarction, researchers reported that hexarelin, a synthetic growth hormone secretagogue given for 21 days, was associated with improved left-ventricular function on MRI, reduced left-ventricular mass and interstitial collagen, lower TGF-beta1 and myofibroblast differentiation, and higher collagen-degrading MMP-13. They also observed a shift toward parasympathetic autonomic balance and lower inflammatory markers. This is one of several concordant rodent infarction studies from this group, which strengthens the preclinical mechanistic story of favorable post-infarct remodeling while remaining entirely animal-based. Limitations include a single-species acute model and modest group sizes. These are preclinical findings; human trials would be needed before any clinical conclusions can be drawn.

Plain-language abstract

Researchers studied hexarelin, a lab-made peptide, in mice that had a heart attack created by tying off a coronary artery. Mice received hexarelin or an inactive vehicle for 21 days. Using MRI, the team found hexarelin-treated mice had better heart pumping function than untreated mice. Their hearts also showed less enlargement and scar tissue, lower levels of proteins that drive scarring, and more of an enzyme that breaks down scar tissue. The animals' nervous-system balance shifted toward the calming branch, and markers of heart injury and inflammation were lower. The authors conclude hexarelin helped the heart recover with less harmful scarring. The abstract reports no adverse events. These are preclinical findings in mice; human studies would be needed before drawing conclusions.