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Tau beyond the Brain: Endoplasmic Reticulum Stress and Tau Phosphorylation as Emerging Drivers of Diabetic Nephropathy

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Author(s)
Kim, Na-YeongOh, Chang-Myung
Type
Article
Citation
Diabetes and Metabolism Journal, v.50, no.5, pp.884 - 886
Issued Date
2026-09
Abstract
Diabetic nephropathy (DN) is the leading cause of end-stage kidney disease worldwide, affecting approximately 40% of all individuals with diabetes mellitus and contributing to a nearly 38% increase in age-standardized mortality rate over the past three decades [1]. Despite notable advances in treatment methods based on renin-angiotensin system blockade and sodiumglucose cotransporter 2 inhibition, a substantial proportion of patients progress to kidney failure, underscoring the need for a deeper understanding of the pathogenic mechanisms that drive glomerular injury and tubular damage. Investigation into potential mediators of renal injury has recently focused on tau, a microtubule-associated protein canonically associated with neurodegenerative tauopathies such as Alzheimer’s disease (AD). In this issue of the Diabetes & Metabolism Journal, Lee et al. [2] provide mechanistic evidence that site-specific tau phosphorylation and endoplasmic reticulum (ER) stress contribute to DN pathogenesis, expanding the scope of therapeutic opportunities.
Publisher
대한당뇨병학회
ISSN
2233-6079
DOI
10.4093/dmj.2026.0620
URI
https://scholar.gist.ac.kr/handle/local/34636
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