Lipocalin-2 Is Induced by Uromodulin Aggregates without Impacting Kidney Disease Progression in Autosomal Dominant Tubulointerstitial Kidney Disease–UMOD

Key Points

• This research aims to explore the role of lipocalin-2 (LCN2) in response to uromodulin aggregates and its implications for kidney disease progression.
• Examined LCN2 induction by uromodulin aggregates and endoplasmic reticulum (ER) stress across various models.
• Analyzed the impact of LCN2 on iron handling and kidney disease pathways.
• LCN2 was induced by intracellular uromodulin aggregates and ER stress.
• Despite LCN2's role in iron handling, it did not promote fibrosis or inflammation.
• LCN2 serves more as a biomarker for protein toxicity than as a viable therapeutic target.