Tubular Mitochondrial Pyruvate Carrier Disruption Elicits Redox Adaptations that Protect from Acute Kidney Injury.
acute kidney injury
metabolomics
mitochondrial metabolism
oxidative damage
Journal
bioRxiv : the preprint server for biology
Titre abrégé: bioRxiv
Pays: United States
ID NLM: 101680187
Informations de publication
Date de publication:
31 Jan 2023
31 Jan 2023
Historique:
pubmed:
14
2
2023
medline:
14
2
2023
entrez:
13
2
2023
Statut:
epublish
Résumé
Energy-intensive kidney reabsorption processes essential for normal whole-body function are maintained by tubular epithelial cell metabolism. Tubular metabolism changes markedly following acute kidney injury (AKI), but which changes are adaptive versus maladaptive remain poorly understood. In publicly available data sets, we noticed a consistent downregulation of the mitochondrial pyruvate carrier (MPC) after AKI, which we experimentally confirmed. To test the functional consequences of MPC downregulation, we generated novel tubular epithelial cell-specific
Identifiants
pubmed: 36778297
doi: 10.1101/2023.01.31.526492
pmc: PMC9915694
pii:
doi:
Types de publication
Preprint
Langues
eng
Subventions
Organisme : NIDDK NIH HHS
ID : R01 DK104998
Pays : United States
Organisme : NCI NIH HHS
ID : P30 CA086862
Pays : United States
Organisme : NICHD NIH HHS
ID : K12 HD027748
Pays : United States
Organisme : NIAMS NIH HHS
ID : R00 AR070914
Pays : United States
Organisme : NIDDK NIH HHS
ID : T32 DK007690
Pays : United States
Organisme : NIDDK NIH HHS
ID : K01 DK126991
Pays : United States
Organisme : NCI NIH HHS
ID : P01 CA217797
Pays : United States
Organisme : NIEHS NIH HHS
ID : P30 ES005605
Pays : United States
Déclaration de conflit d'intérêts
COMPETING INTERESTS The authors declare no competing interests.