{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Jones BA"],"funding":["National Center for Advancing Translational Sciences","NCATS NIH HHS","NIDDK NIH HHS","National Institute of Diabetes and Digestive and Kidney Diseases","National Cancer Institute","NCI NIH HHS"],"pagination":["e181443"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11949063"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["10(5)"],"pubmed_abstract":["Chronic kidney disease (CKD) is associated with renal metabolic disturbances, including impaired fatty acid oxidation (FAO). Nicotinamide adenine dinucleotide (NAD+) is a small molecule that participates in hundreds of metabolism-related reactions. NAD+ levels are decreased in CKD, and NAD+ supplementation is protective. However, both the mechanism of how NAD+ supplementation protects from CKD, as well as the cell types involved, are poorly understood. Using a mouse model of Alport syndrome, we show that nicotinamide riboside (NR), an NAD+ precursor, stimulated renal PPARα signaling and restored FAO in the proximal tubules, thereby protecting from CKD in both sexes. Bulk RNA-sequencing showed that renal metabolic pathways were impaired in Alport mice and activated by NR in both sexes. Thes"],"journal":["JCI insight"],"pubmed_title":["NAD+ prevents chronic kidney disease by activating renal tubular metabolism."],"pmcid":["PMC11949063"],"funding_grant_id":["U54 DK137328","R01DK127830","R01 DK116567","P30 CA051008","P30CA051008","F30 DK129003","TL1TR001431","P50DK133943","U01 DK114923","R01 DK127830","P50 DK133943","R01DK116567","TL1 TR001431","U01DK114923","F30DK129003"],"pubmed_authors":["Eadon MT","Jain S","Sadiq A","Rosenberg AZ","Yoshida T","Jones BA","Myakala K","Santo BA","Levi M","Yang X","Gisch DL","Melo Ferreira R","Panov J","Allen KC","Taranenko E","Korolowicz K","Cheng YH","Wang XX"],"additional_accession":[]},"is_claimable":false,"name":"NAD+ prevents chronic kidney disease by activating renal tubular metabolism.","description":"Chronic kidney disease (CKD) is associated with renal metabolic disturbances, including impaired fatty acid oxidation (FAO). Nicotinamide adenine dinucleotide (NAD+) is a small molecule that participates in hundreds of metabolism-related reactions. NAD+ levels are decreased in CKD, and NAD+ supplementation is protective. However, both the mechanism of how NAD+ supplementation protects from CKD, as well as the cell types involved, are poorly understood. Using a mouse model of Alport syndrome, we show that nicotinamide riboside (NR), an NAD+ precursor, stimulated renal PPARα signaling and restored FAO in the proximal tubules, thereby protecting from CKD in both sexes. Bulk RNA-sequencing showed that renal metabolic pathways were impaired in Alport mice and activated by NR in both sexes. Thes","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Mar","modification":"2026-06-01T10:14:03.622Z","creation":"2025-07-13T03:04:27.99Z"},"accession":"S-EPMC11949063","cross_references":{"pubmed":["40059824"],"doi":["10.1172/jci.insight.181443"]}}