ArticleInternational journal of molecular sciences2023
ER Stress-Perturbed Intracellular Protein O-GlcNAcylation Aggravates Podocyte Injury in Diabetes Nephropathy.
Article in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.
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Who cites it
11 citing papers in PubMed, 1 synthesis or guideline pooled it, 12 citations in OpenAlex.
- Efficacy and potential pharmacological mechanism ofRenal failure · 2025Pooled it
- O-GlcNAcylation: A bridge for regulating the function of the "heart-kidney-bone axis".Biochemistry and biophysics reports · 2026Review
- Unveiling lactylation: A novel frontier in the pathogenesis of diabetic nephropathy (Review).International journal of molecular medicine · 2026Review
- Post‑translational modifications in diabetic kidney disease (Review).International journal of molecular medicine · 2026Review
- Intravenous delivery of mesenchymal stromal cells reverses Müller cell endoplasmic reticulum stress in diabetic retinopathy.Stem cell research & therapy · 2025Article
- Glycosylation in kidney diseases.Precision clinical medicine · 2025Review
- Activation of farnesoid X receptor upregulates binding immunoglobulin protein expression and alleviates diabetic nephropathy.World journal of diabetes · 2025Article
- Immunohistochemical Study onActa histochemica et cytochemica · 2025Review
- Urinary fatty acid-binding protein 4 is a promising biomarker for glomerular damage in patients with diabetes mellitus.Journal of diabetes investigation · 2025Article
- Review
- SGLT2 inhibition attenuates diabetic tubulopathy by suppressing SGK1-mediated pyroptosis.Frontiers in endocrinology · 2025Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Diabetes nephropathy (DN) is the leading cause of end-stage renal disease (ESRD) worldwide, and podocyte injury is the central contributor to the progression of DN. Despite the emerging evidence that has established the importance of podocyte endoplasmic reticulum (ER) stress in the pathogenesis of DN, abnormal protein O-GlcNAcylation is also augmented. Currently, the mechanism associating these two hyperglycemia-induced disorders remains poorly understood. This study intended to elucidate whether ER stress drives hyper-protein O-GlcNAcylation to cause podocyte injury in DN. We used both type 1 and type 2 DN models to confirm the occurrence of ER stress and excessive protein O-GlcNAcylation, and then podocyte purification was also conducted for further investigation. Nephroseq V5 data were mined and in vitro studies were applied to reveal the involvement of ER stress and hyper-O-GlcNAcylation in podocyte injury. Our results indicated that ER stress was induced in both type 1 and type 2 DN, and the human RNA-seq data from Nephroseq V5 showed that O-GlcNAcylation-related genes were significantly upregulated in the DN patients. We further demonstrated that ER stress occurred prior to hyper-O-GlcNAc modification and that pharmacologically inhibited protein O-GlcNAcylation can help decrease the podocyte apoptosis induced by hyperglycemia. Together, these discoveries will aid in uncovering the activation of the ER stress-O-GlcNAcylation axis in podocyte injury under DN, which will help open up new therapeutic approaches for preventing DN progression.
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