ArticleRedox biology2023
DsbA-L interacting with catalase in peroxisome improves tubular oxidative damage in diabetic nephropathy.
Article in Redox biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 20 citations in OpenAlex.
- ZBP1 Mediates Renal Tubular Injury in Diabetic Nephropathy Through RIPK3-mediated Necroptosis.Inflammation · 2026Article
- Hybrid nanovesicles promote diabetic wound healing via dual-targeted multimodal therapy.Burns & trauma · 2026Article
- Imidazole Propionate Induces Kidney Damage by Activating the ROS-NLRP3 Signaling Pathway Through mTOR Inhibition of Autophagy in Renal Tubular Epithelial Cells.Mediators of inflammation · 2026Article
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- The Ferroptosis-Mitochondrial Axis in Depression: Unraveling the Feedforward Loop of Oxidative Stress, Metabolic Homeostasis Dysregulation, and Neuroinflammation.Antioxidants (Basel, Switzerland) · 2025Review
- Reactive Oxygen Species in Asthma: Regulators of Macrophage Polarization and Therapeutic Implications: A Narrative Review.Journal of asthma and allergy · 2025Review
- Identification and Verification of Biomarkers Related to Polyamine Metabolism in Diabetic Nephropathy.Journal of diabetes research · 2025Article
- New insights of DsbA-L in the pathogenesis of metabolic diseases.Molecular and cellular biochemistry · 2024Review
- YAP1 preserves tubular mitochondrial quality control to mitigate diabetic kidney disease.Redox biology · 2024Article
- Enhanced ROS Production and Mitochondrial Metabolic Shifts in CD4International journal of molecular sciences · 2024Article
- Podocyte OTUD5 alleviates diabetic kidney disease through deubiquitinating TAK1 and reducing podocyte inflammation and injury.Nature communications · 2024Article
- Global research hotspots and trends in oxidative stress-related diabetic nephropathy: a bibliometric study.Frontiers in endocrinology · 2024Article
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Authors and funding
15 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Peroxisomes are metabolically active organelles that are known for exerting oxidative metabolism, but the precise mechanism remains unclear in diabetic nephropathy (DN). Here, we used proteomics to uncover a correlation between the antioxidant protein disulfide-bond A oxidoreductase-like protein (DsbA-L) and peroxisomal function. In vivo, renal tubular injury, oxidative stress, and cell apoptosis in high-fat diet plus streptozotocin (STZ)-induced diabetic mice were significantly increased, and these changes were accompanied by a "ghost" peroxisomal phenotype, which was further aggravated in DsbA-L-deficient diabetic mice. In vitro, the overexpression of DsbA-L in peroxisomes could improve peroxisomal phenotype and function, reduce oxidative stress and cell apoptosis induced by high glucose (HG, 30 mM) and palmitic acid (PA, 250 μM), but this effect was reversed by 3-Amino-1,2,4-triazole (3-AT, a catalase inhibitor). Mechanistically, DsbA-L regulated the activity of catalase by binding to it, thereby reducing peroxisomal leakage and proteasomal degradation of peroxisomal matrix proteins induced by HG and PA. Additionally, the expression of DsbA-L in renal tubules of patients with DN significantly decreased and was positively correlated with peroxisomal function. Taken together, these results highlight an important role of DsbA-L in ameliorating tubular injury in DN by improving peroxisomal function.
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