ArticleKidney international reports2024
Oxidative Stress Contributes to Slit Diaphragm Defects Caused by Disruption of Endocytosis.
Article in Kidney international reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 6 citations in OpenAlex.
- Elevated Piezo levels cause structural and functional alterations inLife science alliance · 2026Article
- Integrated transcriptomic analysis of LMB2-induced podocyte injury identifies conserved inflammatory and adaptive stress responses.PloS one · 2026Article
- Interplay of EGFR, JNK, and ROS signaling in soma-germline communication in the Drosophila testis.Stem cell reports · 2025Article
- Cigarette smoke impairs the endocytotic process inToxicology research · 2025Article
- Combined transcriptome and proteome profiling reveal cell-type-specific functions of Drosophila garland and pericardial nephrocytes.Communications biology · 2024Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Introduction: Podocyte slit diaphragms are an important component of the glomerular filtration barrier. Podocyte injury frequently includes defects in slit diaphragms, and various mechanisms for these defects have been described, including altered endocytic trafficking of slit diaphragm proteins or oxidative stress. However, the potential relationship between endocytosis and oxidative stress in the context of slit diaphragm integrity has not been extensively considered. Methods: To examine the potential relationships between endocytosis, oxidative stress, and slit diaphragm integrity, we induced genetic or pharmacological disruption of endocytosis in Results: Disruption of endocytosis in nephrocytes and podocytes led to slit diaphragm defects, elevated levels of ROS (oxidative stress), and activation of the nuclear factor erythroid 2-related factor 2 (Nrf2) antioxidant pathway. In nephrocytes with defective endocytosis, perturbation of Nrf2 signaling exacerbated slit diaphragm defects. Conversely, overexpression of Nrf2 target genes catalase or glucose-6-phosphate dehydrogenase (G6PD) significantly ameliorated slit diaphragm defects caused by disruption of endocytosis. Conclusion: Oxidative stress is an important consequence of defective endocytosis and contributes to the defects in slit diaphragm integrity associated with disruption of endocytic trafficking.
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Registered trials
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