Key result
GHRH agonist MR-356 restores end-diastolic pressure and reverses remodeling in preclinical HFpEF.
Why the study?
To test the efficacy of a synthetic GHRH agonist to improve cardiac performance in cardiometabolic HFpEF using rigorous hemodynamic tools.
Does the GHRH agonist MR-356 improve cardiac performance and reduce pathological remodeling in a murine model of cardiometabolic HFpEF?
Does the GHRH agonist MR-356 improve cardiac performance and reduce pathological remodeling in a murine model of cardiometabolic HFpEF?
p-value: p=<0.01
The synthetic GHRH agonist MR-356 reverses diastolic dysfunction, cardiac hypertrophy, and fibrosis in a cardiometabolic HFpEF murine model, suggesting potential as a novel therapeutic pathway.
This randomized study used rigorous hemodynamic tools to test the efficacy of a synthetic GHRH agonist to improve cardiac performance in a cardiometabolic HFpEF. Daily injection of the GHRH agonist, MR-356, reduced the HFpEF-like effects as evidenced by improved diastolic dysfunction, reduced cardiac hypertrophy, fibrosis, and pulmonary congestion. Notably, end-diastolic pressure and end-diastolic pressure-volume relationship were reset to control levels. Moreover, treatment with MR-356 increased exercise capacity and reduced myocardial stress associated with metabolic inflammation in HFpEF.
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Kanashiro‐Takeuchi et al. (2023) studied Cardiometabolic HFpEF (murine model). MR-356 (synthetic GHRH agonist) vs. Placebo (DMSO + propylene glycol) was evaluated on End-diastolic pressure (EDP) (p=<0.01). Daily injection of the GHRH agonist MR-356 completely restored end-diastolic pressure and reversed cardiac hypertrophy and fibrosis in a murine model of cardiometabolic HFpEF.
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