BRD4 Mediates Cadmium-Induced Oxidative Stress and Kidney Injury in Mice via Disruption of Redox Homeostasis.
Ontology highlight
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 invest
SUBMITTER: Chen J
PROVIDER: S-EPMC12031608 | biostudies-literature | 2025 Mar
REPOSITORIES: biostudies-literature
ACCESS DATA