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Updated: Jun 11, 2025

Acute Kidney Injury Model Induced by Cisplatin in Adult Zebrafish
Published on: May 15, 2021
CDKN1A promotes Cis-induced AKI by inducing cytoplasmic ROS production and ferroptosis
Qian Gao1, Jun-Ming Chen2, Chen-Sui-Zi Li1
1Department of Pharmacy, Shanghai Children's Medical Center, School of Medicine, Shanghai Jiao Tong University, Shanghai, 200127, China; School of Medicine, Shanghai Jiao Tong University, Shanghai, 200125, China.
CDKN1A is identified as a key factor in cisplatin-induced acute kidney injury (AKI). Reducing CDKN1A levels protects kidney cells from damage, suggesting its potential for early AKI diagnosis and treatment.
Area of Science:
- Nephrology
- Molecular Biology
- Bioinformatics
Background:
- Cisplatin chemotherapy can cause acute kidney injury (AKI).
- Early diagnosis and targeted therapies for AKI remain challenging.
- The role of CDKN1A in cisplatin-induced AKI is not well understood.
Purpose of the Study:
- To investigate the role of CDKN1A in cisplatin-induced AKI.
- To evaluate CDKN1A as a potential biomarker for early AKI diagnosis.
- To explore CDKN1A's therapeutic potential in AKI.
Main Methods:
- Bioinformatics analysis of the GSE85957 dataset.
- Machine learning algorithms to identify key genes in cisplatin-induced AKI.
- Experimental validation using human and rat kidney cell lines.
- Quantitative PCR and Western Blotting to assess protein levels.
Main Results:
- CDKN1A was identified as a key gene associated with ferroptosis and the p53 pathway in AKI.
- CDKN1A negatively regulates cell cycle progression (G1/S phase transition).
- Knockdown of CDKN1A reduced cisplatin-induced kidney cell injury, oxidative stress, and ferroptosis.
Conclusions:
- CDKN1A is a promising biomarker for early detection of cisplatin-induced AKI.
- Targeting CDKN1A may offer a novel therapeutic strategy for AKI.
- Integrated bioinformatics and experimental approaches can identify key disease mechanisms and biomarkers.
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