SLC26A1 directs sulfate homeostasis in health and disease
SLC26A1 emerges as a key regulator of sulfate homeostasis, with potential roles in hepatic detoxification, skeletal integrity, and kidney stone disease. Additional mouse models with tissue-specific gene deletion are needed to delineate the role of SLC26A1 in sulfate and oxalate homeostasis as well as disease pathogenesis. Identification of additional patients with damaging variants in SLC26A1 as well as larger population studies may help to elucidate causal relationships of SLC26A1 activity with clinical outcomes.
Authors
- Felix Knauf (ORCID: https://orcid.org/0000-0001-5762-1404)
- Peter S. Aronson (ORCID: https://orcid.org/0000-0002-1860-2419)
- Anna Köttgen (ORCID: https://orcid.org/0000-0002-4671-3714)
- Felix Pitzken
Institutions
- Mayo Clinic (US)
- Johns Hopkins University (US)
- University of Freiburg (DE)
- University Medical Center Freiburg (DE)
- Yale University (US)
- Humboldt-Universität zu Berlin (DE)
- Mayo Clinic in Arizona (US)
- Hypertension Institute (US)
Publication Details
- Journal
- Current Opinion in Nephrology & Hypertension
- Published
- 2025-10-03
- DOI
- https://doi.org/10.1097/mnh.0000000000001123
- Primary Topic
- Ion Transport and Channel Regulation
- Type
- article
- Field-Weighted Citation Impact
- 0.00