CircAASS alleviates renal injury and fibrosis by regulating mitochondrial homeostasis in tubular epithelial cells.

ABSTRACT: Acute kidney injury (AKI) is characterized by the dysfunction of renal tubular epithelial cells (TECs), often leading to renal fibrosis. Mitochondrial impairment is a common hallmark across various types of AKI. However, the potential role of circular RNAs (circRNAs) in modulating mitochondrial homeostasis during AKI and subsequent renal fibrosis remains underexplored. Our findings reveal a significant reduction of circAass levels in the renal cortex across all three AKI models. Mechanistically, circAASS mitigates TEC apoptosis and inflammatory responses by promoting mitochondrial homeostasis, thereby attenuating AKI. Specifically, cytoplasmic circAASS acts as a competing endogenous RNA (ceRNA) by sequestering MIR324-3p, which in turn enhances the expression of

SUBMITTER: Ma T 

PROVIDER: S-EPMC12758326 | biostudies-literature | 2026 Jan

REPOSITORIES: biostudies-literature