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The AE4 transporter mediates kidney acid-base sensing
Publikation: Bidrag til tidsskrift/Konferencebidrag i tidsskrift /Bidrag til avis › Tidsskriftartikel › Forskning › peer review
DOI
- https://doi.org/10.1038/s41467-023-38562-x
Forlagets udgivne version
- Helga Vitzthum, University Medical Center Hamburg-Eppendorf ,
- M Koch, Center for Experimental Medicine, University of Michigan, Ann Arbor, University Medical Center Hamburg-Eppendorf ,
- L Eckermann, University Medical Center Hamburg-Eppendorf ,
- S L Svendsen
- P Berg
- C A Hübner, Department of Psychiatry and Psychotherapy, Jena University Hospital, Jena, Germany. ,
- C A Wagner, National Center of Competence in Research NCCR Kidney.CH ,
- J Leipziger
- C Meyer-Schwesinger, University Medical Center Hamburg-Eppendorf ,
- H Ehmke, University Medical Center Hamburg-Eppendorf
The kidney plays a key role in the correction of systemic acid-base imbalances. Central for this regulation are the intercalated cells in the distal nephron, which secrete acid or base into the urine. How these cells sense acid-base disturbances is a long-standing question. Intercalated cells exclusively express the Na+-dependent Cl-/HCO3- exchanger AE4 (Slc4a9). Here we show that AE4-deficient mice exhibit a major dysregulation of acid-base balance. By combining molecular, imaging, biochemical and integrative approaches, we demonstrate that AE4-deficient mice are unable to sense and appropriately correct metabolic alkalosis and acidosis. Mechanistically, a lack of adaptive base secretion via the Cl-/HCO3- exchanger pendrin (Slc26a4) is the key cellular cause of this derailment. Our findings identify AE4 as an essential part of the renal sensing mechanism for changes in acid-base status.
| Originalsprog | Engelsk |
|---|---|
| Artikelnummer | 3051 |
| Tidsskrift | Nature Communications |
| Vol/bind | 14 |
| Nummer | 1 |
| Sider (fra-til) | 3051 |
| ISSN | 2041-1723 |
| DOI | |
| Status | Udgivet - 26 maj 2023 |
Bibliografisk note
© 2023. The Author(s).
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