Hepatocyte mitochondrial NAD<sup>+</sup> content is limiting for liver regeneration.
Ontology highlight
ABSTRACT: Nicotinamide adenine dinucleotide (NAD+) precursor supplementation shows metabolic and functional benefits in rodent models of disease and is being explored as potential therapeutic strategy in humans. However, the wide range of processes that involve NAD+ in every cell and subcellular compartment make it difficult to narrow down the mechanisms of action. Here we show that the rate of liver regeneration is closely associated with the concentration of NAD+ in hepatocyte mitochondria. We find that the mitochondrial NAD+ concentration in hepatocytes of male mice is determined by the expression of the transporter SLC25A51 (MCART1). The heterozygous loss of SLC25A51 modestly decreases mitochondrial NAD+ content in multiple tissues and impai
SUBMITTER: Mukherjee S
PROVIDER: S-EPMC12727530 | biostudies-literature | 2025 Dec
REPOSITORIES: biostudies-literature
ACCESS DATA