Abstract: FR-PO0378
Dual Bioactive Flavonol-Based Carbonized Quantum Dots Protect Kidneys by Targeting DcR2 to Inhibit Tubular Senescence and Hinder AKI-to-CKD Transition
Session Information
- AKI: Mechanisms - Metabolism and Repair
October 23, 2026 | Location: Exhibit Hall A, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Acute Kidney Injury
- 103 AKI: Mechanisms
Authors
- Chen, Juan, Army Medical University, Chongqing, China
- Wang, Pingping, Army Medical University, Chongqing, China
- Chen, Jia, Army Medical University, Chongqing, China
- He, Yani, Army Medical University, Chongqing, China
- Chen, Kehong, Army Medical University, Chongqing, China
Background
Acute kidney injury (AKI) is a common critical clinical syndrome characterized by rapid renal dysfunction, mainly caused by nephrotoxins and ischemia. No effective targeted therapy exists for AKI. Decoy receptor 2 (DcR2), a TRAIL transmembrane receptor, is significantly upregulated in injured renal tubular cells after AKI. Here, we demonstrate that the biomimetic membrane–QU-CDs–DcR2 antagonistic peptide alleviates post-AKI renal tubular injury.
Methods
DcR2 antagonistic peptides were screened from phage display libraries through three rounds of biopanning against recombinant DcR2 protein, with the optimal candidate identified by mass spectrometry, HPLC and BLI affinity assay. The peptide was encapsulated in senescent renal tubular cell-derived biomimetic membranes to enhance stability and targeting. Dual-active quercetin-carbonized quantum dots (Qu-CDs) were incorporated for real-time fluorescence tracing, enabling integrated diagnosis and therapy. IRI mouse models were established for in vivo evaluation. In vivo imaging tracked the biodistribution of biomimetic membrane–Qu-CDs–DcR2 peptide. HE staining verified the biosafety in major organs, and PAS staining assessed renal pathological lesions. Renal function was evaluated by detecting Scr, BUN and Ucr levels. Renal fibrosis was determined using Masson's trichrome staining and immunostaining for α-SMA, collagen 1 and fibronectin.
Results
HE staining revealed no obvious pathological damage in major organs of the treatment group. Fluorescence imaging confirmed that biomimetic membrane–CDs–DcR2 antagonistic peptide predominantly accumulated in injured kidneys of IRI mice. This formulation significantly alleviated IRI-induced tubular injury and interstitial inflammation, and markedly reversed elevated Scr, BUN and Ucr levels. Furthermore, it effectively attenuated renal fibrosis in the long term.
Conclusion
Our results demonstrate that biomimetic membrane–CDs–DcR2 antagonistic peptide effectively alleviates IRI-induced renal injury and delays AKI-CKD progression, representing a promising therapeutic candidate for AKI.