ArticleToxics2025
BRD4 Mediates Cadmium-Induced Oxidative Stress and Kidney Injury in Mice via Disruption of Redox Homeostasis.
Article in Toxics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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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.
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Who cites it
2 citing papers in PubMed.
- Role of NOX4 and GSH in Cadmium-Induced Renal Redox Homeostatic Dysregulation of Rats and APO Intervention Effect Study.Biological trace element research · 2026Article
- Effects of heavy metal exposure on kidney transplant recipients: mechanisms and clinical implications for graft failure risk.Frontiers in immunology · 2025Review
Corrections and comments
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Authors and funding
9 authors.
Funding
Abstract
Cadmium (Cd) is a toxic heavy metal that threatens public health, with kidney injury being one of the common manifestations after Cd exposure. Oxidative stress plays a crucial role in Cd-induced kidney injury, arising from an imbalance between cellular oxidation and antioxidation processes. Bromodomain-containing protein 4 (BRD4) has been identified as a significant factor in the initiation and advancement of multiple diseases, primarily due to its regulatory role in oxidative stress. Nevertheless, the specific role of BRD4 in Cd-induced kidney oxidative injury remains poorly understood. The present study demonstrates that BRD4 is activated in the kidney after Cd exposure, while JQ1 (a BRD4 inhibitor) treatment inhibits Cd-induced oxidative stress and kidney injury. Subsequently, we investigate the mechanisms by which Cd regulates oxidative stress both in vivo and in vitro. The results indicate that JQ1 treatment reduces the expression levels of NADPH oxidase 4 (Nox4), thereby alleviating mitochondrial damage and reducing reactive oxygen species (ROS) generation. Furthermore, JQ1 treatment facilitates nuclear translocation levels of Nuclear factor erythroid-derived 2-like 2 (Nrf2), thereby enhancing the antioxidant defense system in the kidney after Cd exposure. In conclusion, this study reveals that BRD4 is significantly involved in the process of Cd-induced oxidative damage in the kidney, while inhibiting BRD4 is observed to attenuate ROS generation by regulating Nox4 and enhance ROS scavenging by regulating Nrf2, which, in turn, suppresses the oxidative stress level in the kidney after Cd exposure. These findings suggest that targeting BRD4 may represent an effective strategy for the prevention and treatment of Cd-induced kidney diseases.
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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.