ArticleInternational journal of molecular sciences2020
Underlying Histopathology Determines Response to Oxidative Stress in Cultured Human Primary Proximal Tubular Epithelial Cells.
Article in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed.
- KLF transcription factors in metabolic kidney disease: from podocyte protection to tubulointerstitial fibrosis.International urology and nephrology · 2026Review
- Exploration of zileuton protective mechanisms against vancomycin-associated nephrotoxicity.Toxicology and applied pharmacology · 2025Article
- Metabolite pathway alterations identified by magnetic resonance metabolomics in a proximal tubular epithelial cell line treated with TGF-β1.Physiological reports · 2025Article
- Protection against vancomycin-associated nephrotoxicity by zileuton: role of mitochondria revealed by electron microscopic study.Ultrastructural pathology · 2025Article
- Mitochondrial dysfunction in acute kidney injury.Renal failure · 2024Review
- Oleanolic acid and its analogues: promising therapeutics for kidney disease.Chinese medicine · 2024Review
- Review
- Hypoxic human proximal tubular epithelial cells undergo ferroptosis and elicit an NLRP3 inflammasome response in CD1cCell death & disease · 2022Article
- Adenine overload induces ferroptosis in human primary proximal tubular epithelial cells.Cell death & disease · 2022Article
- Antioxidant Roles of SGLT2 Inhibitors in the Kidney.Biomolecules · 2022Review
- Cellular Senescence: A New Player in Kidney Injury.Hypertension (Dallas, Tex. : 1979) · 2020Review
Corrections and comments
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Authors and funding
10 authors.
Funding
Abstract
Proximal tubular epithelial cells (PTEC) are key players in the progression of kidney diseases. PTEC studies to date have primarily used mouse models and transformed human PTEC lines. However, the translatability of these models to human kidney disease has been questioned. In this study, we investigated the phenotypic and functional response of human primary PTEC to oxidative stress, an established driver of kidney disease. Furthermore, we examined the functional contribution of the underlying histopathology of the cortical tissue used to generate our PTEC. We demonstrated that human primary PTEC from both histologically 'normal' and 'diseased' cortical tissue responded to H
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