Hexarelin treatment preserves myocardial function and reduces cardiac fibrosis in a mouse model of acute myocardial infarction.
McDonald. Hayley H; Peart. Jason J; Kurniawan. Nyoman N; Galloway. Graham G; Royce. Simon S; Samuel. Chrishan S CS; Chen. Chen C
Key Findings
- Hexarelin (0.3 mg/kg/day) improved left‑ventricular function 14 days after myocardial infarction in mice.
- Treatment reduced heart muscle mass, interstitial collagen, and overall fibrosis, linked to lower TGF‑β1 and higher MMP‑13 levels.
- Inflammatory markers (troponin‑I, IL‑1β, TNF‑α) and sympathetic nervous activity were decreased, indicating less heart injury and a shift toward parasympathetic dominance.
Practical Outcomes
- Hexarelin shows promise as a heart‑protective agent after a heart attack, but the evidence is limited to mouse models. For biohackers, it’s not yet a ready‑to‑use supplement; more human safety and dosing data are needed before considering self‑experimentation.
Summary
In mice that had a heart attack, giving the synthetic peptide hexarelin for three weeks helped the heart pump better, reduced scar tissue, lowered inflammation, and shifted the nervous system toward a more relaxed (parasympathetic) state. These effects suggest hexarelin could aid heart healing, but the work was done in animals, not people.
Abstract
Ischemic heart disease (IHD) is a leading cause of morbidity and mortality worldwide. Growth hormone secretagogues (GHS) have been shown to improve cardiac function in models of IHD. This study determined whether hexarelin (HEX), a synthetic GHS, preserves cardiac function and morphology in a mouse model of myocardial infarction (MI). MI was induced by ligation of the left descending coronary artery in C57BL/6J mice followed by vehicle (VEH; n = 10) or HEX (0.3 mg/kg/day; n = 11) administration for 21 days. MI-injured and sham mice (treated with VEH; n = 6 or HEX; n = 5) underwent magnetic resonance imaging for measurement of left ventricular (LV) function, mass and infarct size at 24 h and 14 days post-MI. MI-HEX mice displayed a significant improvement (P < 0.05) in LV function compared with MI-VEH mice after 14 days treatment. A significant decrease in LV mass, interstitial collagen and collagen concentration was demonstrated with chronic HEX treatment (for 21 days), accompanied by a decrease in TGF-β1 expression, myofibroblast differentiation and an increase in collagen-degrading MMP-13 expression levels. Furthermore, heart rate variability analysis demonstrated that HEX treatment shifted the balance of autonomic nervous activity toward a parasympathetic predominance and sympathetic downregulation. This was combined with a HEX-dependent decrease in troponin-I, IL-1β and TNF-α levels suggestive of amelioration of cardiomyocyte injury. These results demonstrate that GHS may preserve ventricular function, reduce inflammation and favorably remodel the process of fibrotic healing in a mouse model of MI and hold the potential for translational application to patients suffering from MI.
Study Information
pubmed
2018
2018-05-01T00:00:00.000Z
10.14814/phy2.13699
16
64