Propofol triggers mitochondria-mediated apoptosis and c-JUN-mediated epithelial-to-mesenchymal transition in human renal tubular epithelial cells.

Propofol is a widely used intravenous anesthetic for the induction and maintenance of general anesthesia. Although clinical observations have suggested potential nephrotoxic effects of propofol, experimental evidence remains limited. In this study, we investigated the renal effects of propofol in vitro using human renal proximal tubular epithelial (HK-2) cells. Our results demonstrate that propofol induces persistent oxidative stress and mitochondrial dysfunction, leading to apoptosis. Notably, propofol activates the JNK/c-JUN signaling pathway, which in turn promotes epithelial-to-mesenchymal transition (EMT), as evidenced by morphological changes and increased expression of mesenchymal markers such as vimentin and Snail. These findings suggest a mechanistic link between prolonged propofol exposure and renal fibrotic responses. Our work highlights the need for greater awareness of propofol-associated renal risks and provides a basis for future research into its underlying molecular mechanisms.