ArticleDiabetes2009
Mechanisms of podocyte injury in diabetes: role of cytochrome P450 and NADPH oxidases.
Article in Diabetes, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 173 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
173 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Lipid Peroxidation in Diabetic Kidney Disease: Mechanism and Natural Solution.International journal of molecular sciences · 2025Pooled it
- Effect of Baoshenfang Formula on Podocyte Injury via Inhibiting the NOX-4/ROS/p38 Pathway in Diabetic Nephropathy.Journal of diabetes research · 2019Trial
- Podocyte Metabolic Flexibility Under Stress Conditions: From Metabolic Adaptation to Maladaptive Responses.Cells · 2026Review
- Overcoming Oxidative Stress in Parkinson's Disease: NADPH Oxidase 4 (NOX4) as a Potential Therapeutic Target.Antioxidants (Basel, Switzerland) · 2026Review
- Rho/ROCK Signaling Pathway in Kidney Diseases: Mechanisms and Therapeutic Perspectives.Biomedicines · 2026Review
- Modulating Renal Fibrosis: The Emerging Role of Hepatocyte Growth Factor.International journal of nephrology · 2026Review
- Alpha-dystroglycan receptor signaling likely influences basement membrane laminin α2 mediated pathology in the stria vascularis of Alport mice.Hearing research · 2025Article
- Podocyte-Specific Expression of the Stress Response Protein REDD1 Is Necessary for Diabetes-Induced Podocytopenia.Diabetes · 2025Article
- Acute hyperglycemia induces podocyte apoptosis by monocyte TNF-α release, a process attenuated by vitamin D and GLP-1 receptor agonists.The Journal of steroid biochemistry and molecular biology · 2025Article
- Petunidin alleviates diabetic nephropathy injury via the inhibition of oxidative stress and ferroptosis through the Keap1/mitoNQO1 pathway.Frontiers in cell and developmental biology · 2025Article
- A human stem cell-derived model reveals pathologic extracellular matrix remodeling in diabetic podocyte injury.Matrix biology plus · 2024Article
- Podocyte-targeted therapies - progress and future directions.Nature reviews. Nephrology · 2024Review
- Oxidative Stress: A Culprit in the Progression of Diabetic Kidney Disease.Antioxidants (Basel, Switzerland) · 2024Review
- Endothelial NOX5 Obliterates the Reno-Protective Effect of Nox4 Deletion by Promoting Renal Fibrosis via Activation of EMT and ROS-Sensitive Pathways in Diabetes.Antioxidants (Basel, Switzerland) · 2024Article
- Nox4-SH3YL1 complex is involved in diabetic nephropathy.iScience · 2024Article
- Arachidonic acid metabolism as a therapeutic target in AKI-to-CKD transition.Frontiers in pharmacology · 2024Review
- A Putative Role for TRPC6 in Immune-Mediated Kidney Injury.International journal of molecular sciences · 2023Review
- Involvement of NADPH oxidases in the Na/K‑ATPase/Src/ROS oxidant amplification loop in renal fibrosis.Molecular medicine reports · 2023Article
- Nox4 as a novel therapeutic target for diabetic vascular complications.Redox biology · 2023Review
- Unraveling the Crosstalk between Lipids and NADPH Oxidases in Diabetic Kidney Disease.Pharmaceutics · 2023Review
113 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
Abstract
objectiveWe investigated the role of cytochrome P450 of the 4A family (CYP4A), its metabolites, and NADPH oxidases both in reactive oxygen species (ROS) production and apoptosis of podocytes exposed to high glucose and in OVE26 mice, a model of type 1 diabetes. RESEARCH DESIGN AND
methodsApoptosis, albuminuria, ROS generation, NADPH superoxide generation, CYP4A and Nox protein expression, and mRNA levels were measured in vitro and in vivo.
resultsExposure of mouse podocytes to high glucose resulted in apoptosis, with approximately one-third of the cells being apoptotic by 72 h. High-glucose treatment increased ROS generation and was associated with sequential upregulation of CYP4A and an increase in 20-hydroxyeicosatetraenoic acid (20-HETE) and Nox oxidases. This is consistent with the observation of delayed induction of NADPH oxidase activity by high glucose. The effects of high glucose on NADPH oxidase activity, Nox proteins and mRNA expression, and apoptosis were blocked by N-hydroxy-N'-(4-butyl-2-methylphenol) formamidine (HET0016), an inhibitor of CYP4A, and were mimicked by 20-HETE. CYP4A and Nox oxidase expression was upregulated in glomeruli of type 1 diabetic OVE26 mice. Treatment of OVE26 mice with HET0016 decreased NADPH oxidase activity and Nox1 and Nox4 protein expression and ameliorated apoptosis and albuminuria.
conclusionsGeneration of ROS by CYP4A monooxygenases, 20-HETE, and Nox oxidases is involved in podocyte apoptosis in vitro and in vivo. Inhibition of selected cytochrome P450 isoforms prevented podocyte apoptosis and reduced proteinuria in diabetes.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.