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Peer-reviewedCC BY 4.0Advanced Science

Kidney‐Targeted Cilastatin Nanoparticles Inhibit DPEP1‐Mediated Ferroptosis for Acute Kidney Injury Therapy

  • Wanbing Qin1
  • Jiaqi Huang1
  • Manting Zhang1
  • Wanchun Yang1
  • Mingwei Xu1
  • Chi Jiang1
  • Jiekai Li1
  • Jinjuan Wen1
  • Qibin Huang1
  • Shiqi Wen1
  • Weidong Wang1,2
  • Junbing He1
1 more authors
  • Qinghua Liu3,4,5
5 affiliations
  1. 1Jieyang Medical Research Center Jieyang People's Hospital Jieyang Guangdong China
  2. 2Department of Pathophysiology Zhongshan School of Medicine Sun Yat‐sen University Guangzhou China
  3. 3Department of Nephrology The First Affiliated Hospital Sun Yat‐sen University Guangzhou Guangdong China
  4. 4Department of Nephrology Jieyang People's Hospital Jieyang Guangdong China
  5. 5Guangdong Provincial Key Laboratory of Nephrology NHC Key Laboratory of Clinical Nephrology (Sun Yat‐sen University) Guangzhou China
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Abstract

Cisplatin‐induced acute kidney injury (CI‐AKI) is a frequent, dose‐dependent complication in patients receiving cisplatin chemotherapy, and effective targeted treatments remain unavailable. The development of targeted therapies for CI‐AKI may improve the efficacy of chemotherapy while mitigating renal toxicity. Given that ferroptosis is a key pathological mechanism in CI‐AKI, targeted drug delivery systems against this process represent a promising therapeutic strategy. Dipeptidase 1 (DPEP1) is highly expressed in renal proximal tubular brush borders and has been associated with ferroptosis regulation and tubular injury. In this study, mesoporous polydopamine nanoparticles (MPDA NPs) were engineered for renal‐targeted delivery of cilastatin sodium (CTT), a specific DPEP1 inhibitor, through L‐serine (L‐Ser) surface modification (CTT/MPDA@L‐Ser NPs). In vitro experiments demonstrated that CTT/MPDA@L‐Ser NPs inhibited the expression of DPEP1 to upregulate the expression of the ferroptosis‐suppressing protein glutathione peroxidase 4 (GPX4), thereby suppressing ferroptosis pathways. In AKI mice, CTT/MPDA@L‐Ser NPs exhibited selective renal accumulation, significantly ameliorating serum creatinine and blood urea nitrogen levels. Collectively, CTT/MPDA@L‐Ser NPs exhibited potent therapeutic efficacy against AKI, presenting a promising strategy for targeted AKI management.

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Cite

BibTeXRIS
BibTeX
@article{qin2026kidneytargeted,
  title = {{Kidney‐Targeted Cilastatin Nanoparticles Inhibit DPEP1‐Mediated Ferroptosis for Acute Kidney Injury Therapy}},
  author = {Wanbing Qin and Jiaqi Huang and Manting Zhang and Wanchun Yang and Mingwei Xu and Chi Jiang and Jiekai Li and Jinjuan Wen and Qibin Huang and Shiqi Wen and Weidong Wang and Junbing He and Qinghua Liu},
  journal = {Advanced Science},
  year = {2026},
  month = aug,
  doi = {10.1002/advs.77090},
  url = {https://doi.org/10.1002/advs.77090},
  note = {CC BY 4.0},
}
RIS
TY  - JOUR
TI  - Kidney‐Targeted Cilastatin Nanoparticles Inhibit DPEP1‐Mediated Ferroptosis for Acute Kidney Injury Therapy
AU  - Wanbing Qin
AU  - Jiaqi Huang
AU  - Manting Zhang
AU  - Wanchun Yang
AU  - Mingwei Xu
AU  - Chi Jiang
AU  - Jiekai Li
AU  - Jinjuan Wen
AU  - Qibin Huang
AU  - Shiqi Wen
AU  - Weidong Wang
AU  - Junbing He
AU  - Qinghua Liu
PY  - 2026
DA  - 2026/08/13
JO  - Advanced Science
DO  - 10.1002/advs.77090
UR  - https://doi.org/10.1002/advs.77090
AB  - Cisplatin‐induced acute kidney injury (CI‐AKI) is a frequent, dose‐dependent complication in patients receiving cisplatin chemotherapy, and effective targeted treatments remain unavailable. The development of targeted therapies for CI‐AKI may improve the efficacy of chemotherapy while mitigating renal toxicity. Given that ferroptosis is a key pathological mechanism in CI‐AKI, targeted drug delivery systems against this process represent a promising therapeutic strategy. Dipeptidase 1 (DPEP1) is highly expressed in renal proximal tubular brush borders and has been associated with ferroptosis regulation and tubular injury. In this study, mesoporous polydopamine nanoparticles (MPDA NPs) were engineered for renal‐targeted delivery of cilastatin sodium (CTT), a specific DPEP1 inhibitor, through L‐serine (L‐Ser) surface modification (CTT/MPDA@L‐Ser NPs). In vitro experiments demonstrated that CTT/MPDA@L‐Ser NPs inhibited the expression of DPEP1 to upregulate the expression of the ferroptosis‐suppressing protein glutathione peroxidase 4 (GPX4), thereby suppressing ferroptosis pathways. In AKI mice, CTT/MPDA@L‐Ser NPs exhibited selective renal accumulation, significantly ameliorating serum creatinine and blood urea nitrogen levels. Collectively, CTT/MPDA@L‐Ser NPs exhibited potent therapeutic efficacy against AKI, presenting a promising strategy for targeted AKI management.
SN  - 2198-3844
ER  -