Key result
Cardiac NAD+ redox imbalance exacerbated systolic and diastolic dysfunction in diabetic mice, while elevation of cardiac NAD+ levels by NAMPT overexpression alleviated cardiac dysfunction.
Why the study?
Diabetic tissues are associated with NAD+ redox imbalance, but whether this imbalance directly causes diabetic heart dysfunction had not been tested.
Population
Streptozotocin-induced diabetic C57BL/6 mice and cardiac-specific Ndufs4 knockout (cKO) mice
Comparison
Altered NAD+ redox balance (Ndufs4 cKO or NAMPT overexpression) vs controls
Design
Animal experimental study
Follow-up
16 weeks
Authors
Loading...
NAD+ restoration may merit testing in diabetic cardiomyopathy models; leaves open whether redox correction improves human cardiac outcomes.
In a mouse model of diabetic cardiomyopathy, NAD+ redox imbalance exacerbates cardiac dysfunction via protein acetylation and phosphorylation, while restoring NAD+ levels with NAMPT overexpression is protective.
Chiao et al. (2020) studied Diabetic cardiomyopathy. Altered NAD+ redox balance (Ndufs4-KO and NAMPT overexpression) vs. Wildtype/control mice was evaluated on Cardiac function (systolic and diastolic) and NAD+/NADH ratio. Cardiac NAD+ redox imbalance exacerbated systolic and diastolic dysfunction in diabetic mice, while elevation of cardiac NAD+ levels by NAMPT overexpression alleviated cardiac dysfunction.
Synapse has enriched 2 closely related papers on similar clinical questions. Consider them for comparative context: