Trehalose activates autophagy to alleviate cisplatin-induced chronic kidney injury by targeting the mTOR-dependent TFEB signaling pathway.

ABSTRACT: Rationale: Cisplatin is a potent chemotherapeutic agent limited by significant nephrotoxicity. Multiple cycles of cisplatin administration are necessary to confer chronic disease. Autophagy is a lysosomal degradation pathway that enables the clearance and reuse of cytoplasmic components and is essential for maintaining the integrity and normal physiological function of tissues and organs. However, the precise role of autophagy in renal fibrosis has been controversial. Trehalose, a well-known autophagy inducer, plays a cytoprotective role under various stress conditions, such as oxidative damage, dehydration, and temperature changes. In this study, we established a model of cisplatin-induced chronic kidney disease (CKD) and human renal tubular epithelial cells (HK2) injury to investi

SUBMITTER: Yang J 

PROVIDER: S-EPMC11840734 | biostudies-literature | 2025

REPOSITORIES: biostudies-literature