ArticleToxicology research2023
Di(2-ethylhexyl) phthalate mediates oxidative stress and activates p38MAPK/NF-kB to exacerbate diabetes-induced kidney injury in vitro and in vivo models.
Article in Toxicology research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 13 citations in OpenAlex.
- Di(2-Ethylhexyl) Phthalate Exposure and Risk of Diabetic Kidney Disease: Epidemiological Association and Mechanistic Insights.Diabetes/metabolism research and reviews · 2026Article
- Plastic-Derived Pollutants as Emerging Modifiers of Viral Diseases.Pathogens (Basel, Switzerland) · 2026Review
- The impact of Di(2-ethylhexyl) phthalate on human organ development: mechanisms and clinical relevance review.Frontiers in public health · 2026Review
- Urinary and circulatory levels of plasticizer metabolites and their associations with renal function: a cross-sectional analysis of the NHANES cohort.Annals of medicine · 2025Article
- Network Toxicology and Molecular Docking Reveal the Toxicological Mechanisms of DEHP in Bone Diseases.International journal of molecular sciences · 2025Article
- Nephrotoxicity of Phthalates: A Review Based on Epidemiological and Toxicological Evidence.Toxics · 2025Review
- Investigation of protective effects of rutin\cyclodextrin inclusion complex against testicular damage caused by diisononyl phthalate in rats.Iranian journal of basic medical sciences · 2025Article
- Tempol Mitigates Methotrexate-Induced Osteotoxicity via Oxidative Stress Modulation and MAPK Pathway Inhibition.Drug design, development and therapy · 2025Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Plasticizer di(2-ethylhexyl) phthalate (DEHP) is employed to make polyethylene polymers. Some studies in epidemiology and toxicology have shown that DEHP exposure over an extended period may be hazardous to the body, including nephrotoxicity, and aggravate kidney damage in the context of underlying disease. However, studies on the toxicity of DEHP in diabetes-induced kidney injury have been rarely reported. Using a high-fat diet (HFD) and streptozotocin (STZ, 35 mg/kg)-induced kidney injury in mice exposed to various daily DEHP dosages, we explored the impacts of DEHP on diabetes-induced kidney injury. We discovered that DEHP exposure significantly promoted the renal inflammatory response and oxidative stress in mice, with increased P-p38 and P-p65 protein levels and exacerbated the loss of podocin. The same findings were observed in vitro after stimulation of podocytes with high glucose (30 mmol/L) and exposure to DEHP. Our results suggest that DEHP exacerbates diabetes-induced kidney injury by mediating oxidative stress and activating p38MAPK/NF-κB.
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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 Socratic graph.