10-HDA ameliorates cadmium-induced renal injury by modulating mitochondrial autophagy via the PINK1/Parkin pathway

Cadmium (Cd) is a persistent heavy metal that induces kidney injury with no effective treatment available. 10-Hydroxy-2-decenoic acid (10-HDA) possesses anti-inflammatory and antioxidant properties, yet its role in Cd-induced nephrotoxicity remains unknown. This study investigated whether 10-HDA protects against Cd-induced renal damage. Methods: Mice exposed to Cd via drinking water were treated with 10-HDA. Renal injury was evaluated by histology, immunoblotting, electron microscopy, and mitochondrial membrane potential assays. Results: Cd exposure caused renal tubular injury, oxidative stress, and mitochondrial dysfunction. 10-HDA treatment alleviated these pathological changes, restored ATP levels and mitochondrial membrane potential, and modulated autophagy-related proteins including LC3-II/I, p62, PINK1, and Parkin. These findings indicate that 10-HDA promotes mitophagy via the PINK1/Parkin pathway and effectively attenuates Cd-induced nephrotoxicity, suggesting its potential as a dietary agent for protection against cadmium exposure.