Catalytic activity tunable ceria nanoparticles prevent chemotherapy-induced acute kidney injury without interference with chemotherapeutics

Qinjie Weng, Heng Sun, Chunyan Fang, Fan Xia, Hongwei Liao, Jiyoung Lee, Jincheng Wang, An Xie, Jiafeng Ren, Xia Guo, Fangyuan Li, Bo Yang and Daishun Ling ()
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Qinjie Weng: Zhejiang University
Heng Sun: Zhejiang University
Chunyan Fang: Zhejiang University
Fan Xia: Zhejiang University
Hongwei Liao: Zhejiang University
Jiyoung Lee: Zhejiang University
Jincheng Wang: Zhejiang University
An Xie: Zhejiang University
Jiafeng Ren: Zhejiang University
Xia Guo: Zhejiang University
Fangyuan Li: Zhejiang University
Bo Yang: Zhejiang University
Daishun Ling: Zhejiang University

Nature Communications, 2021, vol. 12, issue 1, 1-14

Abstract: Abstract Acute kidney injury (AKI) is a prevalent and lethal adverse event that severely affects cancer patients receiving chemotherapy. It is correlated with the collateral damage to renal cells caused by reactive oxygen species (ROS). Currently, ROS management is a practical strategy that can reduce the risk of chemotherapy-related AKI, but at the cost of chemotherapeutic efficacy. Herein, we report catalytic activity tunable ceria nanoparticles (CNPs) that can prevent chemotherapy-induced AKI without interference with chemotherapeutic agents. Specifically, in the renal cortex, CNPs exhibit catalytic activity that decomposes hydrogen peroxide, and subsequently regulate the ROS-involved genes by activating the Nrf2/Keap1 signaling pathway. These restore the redox homeostasis for the protection of kidney tubules. Under an acidic tumor microenvironment, CNPs become inert due to the excessive H+ that disrupts the re-exposure of active catalytic sites, allowing a buildup of chemotherapy-mediated ROS generation to kill cancer cells. As ROS-modulating agents, CNPs incorporated with context-dependent catalytic activity, hold a great potential for clinical prevention and treatment of AKI in cancer patients.

Date: 2021
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DOI: 10.1038/s41467-021-21714-2

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