Silencing RPL11 attenuates acute kidney injury by suppressing tubular apoptosis and macrophage-driven inflammation.

ABSTRACT:

Background

Acute kidney injury (AKI) remains a life-threatening syndrome with elusive molecular drivers. Although ribosomal proteins such as RPL11 are increasingly recognized for their extra-ribosomal functions, their roles in AKI pathogenesis remain unexplored.

Methods

The comprehensive multi-omics analysis of mouse AKI kidneys combined scRNA-seq and RNA-seq to identify core regulatory factors. Based on cisplatin induced AKI, a HK-2 cell model was established by siRNA transfection silencing RPL11, while in vivo kidney targeted silencing was achieved using LyP-1 modified nanoparticles encapsulating si-RPL11. Technologies such as Western blotting, qPCR, and IVS fluorescence imaging ensure the successful construction of cell and animal models. Functional testing include

SUBMITTER: Dong Q 

PROVIDER: S-EPMC12394147 | biostudies-literature | 2025

REPOSITORIES: biostudies-literature