ORIGINAL RESEARCH article
Front. Immunol.
Sec. Systems Immunology
Volume 16 - 2025 | doi: 10.3389/fimmu.2025.1642446
This article is part of the Research TopicExploring the Applications of Artificial Intelligence in Disease Screening, Diagnosis, Treatment, and NursingView all 7 articles
Silencing RPL11 Attenuates Acute Kidney Injury by Suppressing Tubular Apoptosis and Macrophage-Driven Inflammation
Provisionally accepted
- The Affiliated Lihuili Hospital of Ningbo University, Ningbo, China
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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.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 includes CCK-8, EdU assay, flow cytometry, TUNEL assay, qPCR, ELISA, and histopathological techniques to evaluate cell proliferation, apoptosis, and inflammatory cytokine levels.Results: RPL11 was identified as the core gene with AKI-specific upregulation in proximal tubules. RPL11 expression correlated with AKI severity and showed positive associations with Scr/KIM-1. The specific silencing of RPL11 in HK-2 cells was successfully induced and the LYS-1 peptide-modified cationic liposome nanoparticles were stable in quality and could target the renal tissue of AKI mice to silence RPL11.The experimental results have jointly confirmed that RPL11 suppressed proliferation, accelerated apoptosis, amplified inflammation and aggravated tubular necrosis and CD68 macrophage infiltration in vitro and in vivo.RPL11 drives AKI progression by orchestrating tubular dysfunction, apoptosis, and immune dysregulation. Our renal-targeted nano-intervention validates RPL11 as a therapeutically actionable target, providing a novel strategy for biomarkerguided AKI management.
Keywords: RPL11, acute kidney injury (AKI), tubular dysfunction, nanoparticle targeting, Immune dysregulation
Received: 06 Jun 2025; Accepted: 25 Jul 2025.
Copyright: © 2025 Dong, Xu, Xu, Liu and Shen. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence: Qian Dong, The Affiliated Lihuili Hospital of Ningbo University, Ningbo, China
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