ArticleFrontiers in immunology2025
Silencing RPL11 attenuates acute kidney injury by suppressing tubular apoptosis and macrophage-driven inflammation.
Article in Frontiers in immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Surfactant protein A (SP-A) alleviates acute kidney injury by reducing macrophage recruitment and M1 polarization.Journal of molecular histology · 2026Article
- The crucial role of N6-methyladenosine modification in acute kidney injury: mechanisms and therapeutic potential.Frontiers in immunology · 2026Review
- Integrated Transcriptomic and Machine Learning Analyses Identify KCNN3 and TLR10 as Candidate Cell-Type-Associated Molecules in Idiopathic Membranous Nephropathy.International journal of general medicine · 2026Article
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Authors and funding
6 authors.
Funding
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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 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 Conclusion: 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 biomarker-guided AKI management.
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