What is the clinical evidence from this study?

Study design: Other. Population: Eccentric cardiac hypertrophy. Intervention: Cardiac-specific SLC25A51 knockout vs. Control mice. Primary outcome: mtNAD+ levels, cardiac hypertrophy, and survival.

October 9, 2025Circulation Research

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

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Key result

Cardiac SLC25A51 knockout depletes mtNAD+ by ~85%, driving severe eccentric hypertrophy and early death.

Population

Cardiac-specific SLC25A51 knockout (cKO) mice and control mice

Comparison

Cardiac-specific knockout of SLC25A51 vs Control mice

Design

Preclinical

Follow-up

up to 8 weeks of age

Authors

WZWeronika ZarzyckaOklahoma Medical Research Foundation JCJoseph M. CaswellHealth Sciences North KKKamil KobakOklahoma Medical Research Foundation

Discussion

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Implication

SLC25A51 is indispensable for maintaining the mitochondrial NAD+ pool in the heart and is essential for postnatal cardiac metabolic adaptations and survival.

Key Points

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.

Structured PICO

Population

Cardiac-specific SLC25A51 knockout mice and control mice followed up to 8 weeks of age.

Intervention

Cardiac-specific knockout of SLC25A51

Comparator

Control mice

Outcome

Postnatal changes in cardiac metabolism and function, including growth, survival, cardiac hypertrophy, and mtNAD+ levelssurrogate

SLC25A51 is indispensable for maintaining the mitochondrial NAD+ pool in the heart and is essential for postnatal cardiac metabolic adaptations and survival.

Cite This Study

Zarzycka et al. (2025) studied Eccentric cardiac hypertrophy. Cardiac-specific SLC25A51 knockout vs. Control mice was evaluated on mtNAD+ levels, cardiac hypertrophy, and survival. Cardiac-specific SLC25A51 knockout in mice depleted mtNAD+ levels by ~85%, resulting in pronounced eccentric cardiac hypertrophy, retarded growth, and premature death by 8 weeks of age.

synapsesocial.com/papers/68e80eb363e2e2f707877d64 https://doi.org/10.1161/res.137.suppl_1.fri132

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Implication

SLC25A51 is indispensable for maintaining the mitochondrial NAD+ pool in the heart and is essential for postnatal cardiac metabolic adaptations and survival.

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

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

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

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

Also Consider

Also Consider