Administration of β-Nicotinamide Mononucleotide Attenuates Myocardial Dysfunction in Tail-Suspended Mice.

Microgravity conditions cause myocardial atrophy and dysfunction with limited therapeutics. Accumulating evidence demonstrates that the deficiency of nicotinamide adenine dinucleotide (NAD) contributes to myocardial dysfunction under microgravity, making NAD boosting an appealing therapeutic approach. In this study, we sought to investigate whether β-nicotinamide mononucleotide (NMN), a precursor of NAD, preserved cardiomyocytes size and myocardial function during microgravity. Simulated microgravity was induced by tail-suspension in C57BL/6 mice for 28 days. NMN (100 mg/kg body weight) was given every other day after the onset of tail-suspension. Tail-suspension reduced the NAD content in hearts and decreased the heart weight and cardiomyocytes size, and cardiac function. Administration of NMN attenuates myocardial atrophy and preserves myocardial function in tail-suspended mice. These cardioprotective effects of NAD repletion were associated with the reduction of oxidative stress and improvement of autophagic flux. These findings indicate that NMN may hold great potential as a therapeutic approach for myocardial abnormalities under microgravity conditions.