Lipocalin-2 Is Induced by Uromodulin Aggregates without Impacting Kidney Disease Progression in Autosomal Dominant Tubulointerstitial Kidney Disease–UMOD
LCN2 was induced by intracellular uromodulin aggregates and ER stress in various models of ADTKD-UMOD. Although it influenced iron handling, LCN2 did not drive fibrosis or inflammation, supporting a role as a biomarker of toxic proteinopathy rather than a therapeutic target.
Authors
- Olivier Devuyst (ORCID: https://orcid.org/0000-0003-3744-4767)
- Guglielmo Schiano (ORCID: https://orcid.org/0000-0002-3549-7796)
- Marta Mariniello (ORCID: https://orcid.org/0000-0002-8254-3505)
- Jennifer Lake (ORCID: https://orcid.org/0000-0002-9617-7438)
- Eric Olinger (ORCID: https://orcid.org/0000-0003-1178-7980)
- H Mabillard
- Qin Guo (ORCID: https://orcid.org/0009-0003-2943-0688)
- Fabiola Terzi
- John A. Sayer
Institutions
- Centre National de la Recherche Scientifique (FR)
- Cliniques Universitaires Saint-Luc (BE)
- Inserm (FR)
- University of Zurich (CH)
- Université Paris Cité (FR)
- Newcastle upon Tyne Hospitals NHS Foundation Trust (GB)
- Institut Necker Enfants Malades (FR)
- NIHR Newcastle Biomedical Research Centre (GB)
- University of Newcastle Australia (AU)
- Newcastle University (GB)
Publication Details
- Journal
- Journal of the American Society of Nephrology
- Published
- 2026-03-26
- DOI
- https://doi.org/10.1681/asn.0000001077
- Primary Topic
- Acute Kidney Injury Research
- Type
- article
- Field-Weighted Citation Impact
- 0.00