NAD(+) precursor treatment prevents cardiomyopathy but disrupts erythroid maturation in mitochondrial progeria.
- Open access
NAD+ precursor treatment improves cardiac function but impairs erythroid maturation in mitochondrial progeria mice, revealing tissue-specific effects.
- Why it matters: Understanding the long-term and tissue-specific impacts of NAD+ boosting therapies is crucial for developing safe treatments for degenerative diseases involving mitochondrial dysfunction.
- What they did: Researchers supplemented mutator mice with nicotinamide riboside (NR) and analyzed effects on different tissues, focusing on metabolic and cellular changes in bone marrow, blood, and heart.
- The result: NR treatment enhanced cardiac contractility and normalized metabolism in the heart but caused reductive stress, disrupted heme biosynthesis, and worsened anemia by impairing erythroid maturation, highlighting the need for targeted metabolic interventions.