ArticleScientific reports2020
High glucose induces phosphorylation and oxidation of mitochondrial proteins in renal tubular cells: A proteomics approach.
Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.
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Who cites it
23 citing papers in PubMed, 1 synthesis or guideline pooled it, 37 citations in OpenAlex.
- Mitochondrial Dysfunction in Individuals with Diabetic Kidney Disease: A Systematic Review.Cells · 2022Pooled it
- South African Herbal Teas and Diabetes-Mediated Mitochondrial Dysfunction: Emerging Evidence and Mechanistic Insights.Journal of food science · 2026Review
- Carnitine dysregulation in diabetic kidney disease: from pathogenic mechanism to precision biomarker.Journal of translational medicine · 2026Review
- Post‑translational modifications in diabetic kidney disease (Review).International journal of molecular medicine · 2026Review
- Mitochondrial dysfunction: the hidden catalyst in chronic kidney disease progression.Renal failure · 2025Review
- Aucubin ameliorates diabetic kidney disease by restoring hGENCs autophagy through promoting phosphorylation of ATG4B protein.Renal failure · 2025Article
- 14-3-3ζ: an optimal housekeeping protein for western blot analysis in swine rotator cuff tendon studies.Molecular and cellular biochemistry · 2025Article
- Stallion spermatozoa express LDH isoforms A, B, and C, with LDHC playing a crucial role in sustaining sperm viability.Reproduction (Cambridge, England) · 2025Article
- Mitochondrial Dysfunction in Diabetic Periodontitis: Mechanisms and Therapeutic Potential.Journal of inflammation research · 2025Review
- Role of metabolic conditions in cardiorenal diseases: initiating pathways and therapeutic targeting.Frontiers in nutrition · 2025Review
- Mathurameha ameliorates cardiovascular complications in high-fat diet/low-dose streptozotocin-induced type 2 diabetic rats: insights from histological and proteomic analysis.Journal of molecular histology · 2024Article
- Association of dietary antioxidant indices with kidney function indicators in patients with type 2 diabetes: a cross-sectional study.Scientific reports · 2024Article
- The Renoprotective Mechanisms of Sodium-Glucose Cotransporter-2 Inhibitors (SGLT2i)-A Narrative Review.International journal of molecular sciences · 2024Review
- Obesity, diabetes mellitus, and cardiometabolic risk: An Obesity Medicine Association (OMA) Clinical Practice Statement (CPS) 2023.Obesity pillars · 2023Article
- Peroxiredoxin 6 alleviates high glucose-induced inflammation and apoptosis in HK-2 cells by inhibiting TLR4/NF-κB signaling.Annals of translational medicine · 2023Article
- Glucose fluctuation promotes mitochondrial dysfunctions in the cardiomyocyte cell line HL-1.PloS one · 2023Article
- Proteomic and computational analyses followed by functional validation of protective effects of trigonelline against calcium oxalate-induced renal cell deteriorations.Computational and structural biotechnology journal · 2023Article
- Molecular Pathways of Diabetic Kidney Disease Inferred from Proteomics.Diabetes, metabolic syndrome and obesity : targets and therapy · 2023Review
- Tubular Mitochondrial Dysfunction, Oxidative Stress, and Progression of Chronic Kidney Disease.Antioxidants (Basel, Switzerland) · 2022Review
- Single-Cell Analysis of CHO Cells Reveals Clonal Heterogeneity in Hyperosmolality-Induced Stress Response.Cells · 2022Article
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5 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Mitochondrial dysfunction has been thought to play roles in the pathogenesis of diabetic nephropathy (DN). However, precise mechanisms underlying mitochondrial dysfunction in DN remained unclear. Herein, mitochondria were isolated from renal tubular cells after exposure to normal glucose (5.5 mM glucose), high glucose (25 mM glucose), or osmotic control (5.5 mM glucose + 19.5 mM mannitol) for 96 h. Comparative proteomic analysis revealed six differentially expressed proteins among groups that were subsequently identified by tandem mass spectrometry (nanoLC-ESI-ETD MS/MS) and confirmed by Western blotting. Several various types of post-translational modifications (PTMs) were identified in all of these identified proteins. Interestingly, phosphorylation and oxidation were most abundant in mitochondrial proteins whose levels were exclusively increased in high glucose condition. The high glucose-induced increases in phosphorylation and oxidation of mitochondrial proteins were successfully confirmed by various assays including MS/MS analyses. Moreover, high glucose also increased levels of phosphorylated ezrin, intracellular ATP and ROS, all of which could be abolished by a p38 MAPK inhibitor (SB239063), implicating a role of p38 MAPK-mediated phosphorylation in high glucose-induced mitochondrial dysfunction. These data indicate that phosphorylation and oxidation of mitochondrial proteins are, at least in part, involved in mitochondrial dysfunction in renal tubular cells during DN.
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