Deletion of Kcnj16 altered transcriptomic and metabolomic profiles of Dahl salt-sensitive rats.
Ontology highlight
ABSTRACT: The inwardly rectifying K+ channel Kir5.1 (Kcnj16) is essential in renal salt handling and blood pressure control. However, the underlying mechanisms are not fully understood. Here, we integrated transcriptomics and metabolomics to comprehensively profile the changes in genes and metabolites in the Dahl salt-sensitive (SS) rat lacking Kcnj16 to identify potential mechanisms. Consistent with the phenotype of knockout (KO) rats, the transcriptomic profile predicted reduced blood pressure, kidney damage, and increased ion transport. Canonical pathway analysis suggested activation of metabolic-related pathways while suppression of immune response-related pathways in KO rats. Untargeted metabolomic analysis revealed different metabolic profiles between wild-t
SUBMITTER: Xu B
PROVIDER: S-EPMC11424968 | biostudies-literature | 2024 Oct
REPOSITORIES: biostudies-literature
ACCESS DATA