Molybdenum-bridged endo-exogenous antioxidant synergy reverses acute kidney injury via mitochondrial homeostasis reconstruction.

ABSTRACT: Acute kidney injury (AKI) progression is driven by mitochondrial redox collapse in proximal tubular epithelial cells (PTECs), where reactive oxygen species (ROS) surge and molybdenum (Mo) metabolic dysregulation create an "oxidative storm-defense collapse" cycle. Conventional antioxidant therapies fail to halt AKI chronicity due to their inability to restore Mo-dependent detoxification enzymes (e.g., Mo-containing Amidoxime Reducing Component, mARC). To address this dual pathology, we developed N-acetylcysteine (NAC)-modified molybdenum disulfide quantum dots (NMDs) that implement an endo-exogenous antioxidant collaborative strategy, synergizing exogenous ROS elimination with endogenous Mo enzyme restoration. NMDs achieve triple-tiered targeting: 1) Organ-selective accumulation leveraging

SUBMITTER: Chen Q 

PROVIDER: S-EPMC12628060 | biostudies-literature | 2025 Dec

REPOSITORIES: biostudies-literature