Observational study finds lipocalin-2 induced by uromodulin aggregates, suggesting a biomarker role in kidney disease.
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.
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Lake et al. (2026) studied this question.
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