Key result
NNMT inhibition with AMO-NAM improved cardiac function, reduced LV hypertrophy and fibrosis, and decreased pro-inflammatory gene expression in a HFpEF mouse model.
Why the study?
HFpEF has limited treatment options, and NNMT inhibition was investigated as a potential novel therapeutic option.
Does NNMT inhibition with AMO-NAM improve cardiac function and structure in a mouse model of HFpEF?
Population
Aged female mice with a cardiometabolic HFpEF phenotype
Comparison
NNMT inhibitor AMO-NAM added to HFD vs untreated HFpEF model
Design
Preclinical animal study
Follow-up
Four weeks
Authors
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Animal data support NNMT inhibition in HFpEF; leaves open translation to patients.
Does NNMT inhibition with AMO-NAM improve cardiac function and structure in a mouse model of HFpEF?
NNMT inhibition with AMO-NAM improves cardiac function, reduces hypertrophy and fibrosis, and decreases inflammation in a mouse model of HFpEF, suggesting a potential novel therapeutic target.
Li et al. (2025) studied Heart failure with preserved ejection fraction (HFpEF). AMO-NAM vs. Untreated HFpEF model was evaluated on Cardiac function, structure, and metabolite levels. NNMT inhibition with AMO-NAM improved cardiac function, reduced LV hypertrophy and fibrosis, and decreased pro-inflammatory gene expression in a HFpEF mouse model.
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