Abstract Fri132: mtNAD+ Depletion in Cardiomyocytes Disrupts Postnatal Metabolic Adaptations and Leads to Lethal Eccentric Cardiac Hypertrophy

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Discussion

Knockout of SLC25A51 negatively impacts heart function and metabolism in cardiomyocytes, indicating its crucial role.

Depletion of mtNAD+ in cardiomyocytes leads to lethal eccentric cardiac hypertrophy and disturbed metabolic adaptations.
cKO mice showed an 85% reduction in mtNAD+ levels, significantly slower heart rates, and disrupted TCA cycle function.
Analysis revealed upregulation of fetal contractile genes, indicating a regression in cardiac maturation due to mtNAD+ loss.
SLC25A51 is critical for maintaining mtNAD+ levels, essential for optimal mitochondrial function and cardiac development.

Zarzycka et al. (2025) studied this question.

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