Heart failure & cardiomyopathies
Raising NAD + Level Stimulates Short-Chain Dehydrogenase/Reductase Proteins to Alleviate Heart Failure Independent of Mitochondrial Protein Deacetylation
Authors' conclusion
These findings identify SDR proteins as important regulators of mitochondrial function and molecular targets of NAD+-based therapy.
Study context
- Population
- Mice with established cardiac dysfunction induced by pressure overload; human failing hearts
- Comparison
- Knockout vs Wild-type
Methodological detailsTreatment initiated in mice with established cardiac dysfunction
- Treatment initiated in mice with established cardiac dysfunction
Main finding
As reported in the abstract
- Nicotinamide riboside chloride improved mitochondrial function and blunted HF progression
- Similar benefits in wild-type and knockout mice
- Boosting NAD+ improved function of NAD(H) redox-sensitive SDR family proteins
- Mrpp2 upregulation improves mitochondrial DNA transcript processing and electron transport chain function
- Activation of retinol-pathway SDRs stimulates RXRα/PPARα signaling and restores mitochondrial oxidative metabolism
- Mrpp2 downregulation and impaired mitochondrial ribonuclease P in human failing hearts
Original publication
Raising NAD + Level Stimulates Short-Chain Dehydrogenase/Reductase Proteins to Alleviate Heart Failure Independent of Mitochondrial Protein Deacetylation. Circulation. Published 15 November 2023. doi:10.
Summarised from the published abstract; every number is checked against it