ArticleDiabetes & metabolism journal2026
Interactions between Tau Phosphorylation and Endoplasmic Reticulum Stress in Diabetic Nephropathy.
Article in Diabetes & metabolism journal, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Targeting the PD-L1-induced PDK4/GLS metabolic axis overcomes anti-PD-1 resistance in non-small cell lung cancer.Journal for immunotherapy of cancer · 2026Article
- Tau beyond the Brain: Endoplasmic Reticulum Stress and Tau Phosphorylation as Emerging Drivers of Diabetic Nephropathy.Diabetes & metabolism journal · 2026Article
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Authors and funding
7 authors.
Funding
Abstract
backgruoundTau is a microtubule-associated protein whose abnormal phosphorylation disrupts the cytoskeleton and induces cell death. While its role is well known in neurodegenerative diseases, its function in kidney pathology, particularly diabetic nephropathy (DN), is not well understood.
methodsDN was induced in NADPH oxidase 5 (NOX5) pod+ mice through a high-fat diet (HFD; 60% kcal fat) for 3, 6, and 12 weeks. Kidney tissues and cultured mesangial cells were analyzed for tau phosphorylation at specific residues (Ser202 and Thr205), fibrosis markers (e.g., α-smooth muscle actin), and endoplasmic reticulum (ER) stress. Tau phosphorylation was modulated using thousand and one amino acid kinase inhibitor and ER stress inhibitors. Immunohistochemistry was also performed on human renal biopsy samples from DN patients.
resultspTau Ser202 and Thr205 expression levels were elevated by 6 weeks of the HFD and remained persistently upregulated at 12 weeks. Human biopsy analysis further revealed elevated pTau Ser202 and Thr205 expression in the patients with DN, which correlated with proteinuria. In NOX5 pod+ mice, early metabolic changes developed by HFD led to tau phosphorylation and kidney damage. Transforming growth factor β-induced fibrosis or thapsigargin-induced ER stress increased tau phosphorylation, while inhibiting tau phosphorylation or ER stress alleviated mesangial cell damage.
conclusionOur findings demonstrate that site-specific tau phosphorylation is associated with renal injury in DN and may serve as a potential marker of disease severity. The interplay between tau phosphorylation and ER stress appears to contribute to disease progression. Targeting tau phosphorylation and its upstream stress pathways may offer new therapeutic strategies for DN.
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