Key result
Intact NNT in mice promoted worse diastolic dysfunction after HFD+L-NAME feeding compared to NNT loss-of-function (E/e' ratio 42.8 vs 21.5, P=1.2x10^-10).
Why the study?
HFpEF management lacks disease-modifying therapies, and C57BL6/J mice unexpectedly exhibit less diastolic dysfunction in response to the HFD+L-NAME model.
Comparison
Nnt+/+ vs Nnt-/- challenged with HFD+L-NAME
Design
Preclinical animal model study
Follow-up
9 weeks
Authors
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NNT modulation warrants preclinical testing in HFpEF; hypothesis-generating for mitochondrial targets with no clinical implications yet.
Absolute Event Rate: 42.8% vs 21.5%
p-value: p=1.2×10^-10
Intact mitochondrial NNT promotes diastolic dysfunction and pathological remodeling in a mouse model of cardiometabolic HFpEF, suggesting NNT and Fgf1 as potential therapeutic targets.
Pepin et al. (2025) studied Heart failure with preserved ejection fraction (HFpEF). Intact NNT (Nnt+/+) vs. Nnt loss-of-function (Nnt-/-) was evaluated on E/e' (early diastolic pulse-wave velocity to mitral annular velocity ratio) (p=1.2×10^-10). Intact NNT in mice promoted worse diastolic dysfunction after HFD+L-NAME feeding compared to NNT loss-of-function (E/e' ratio 42.8 vs 21.5, P=1.2x10^-10).
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