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Updated: Mar 21, 2026
Acute Kidney Injury Model Induced by Cisplatin in Adult Zebrafish
Published on: May 15, 2021
CXCL16 regulates cisplatin-induced acute kidney injury
Hua Liang1,2, Zhengmao Zhang1, Liqun He3
1Selzman Institute for Kidney Health and Section of Nephrology, Department of Medicine, Baylor College of Medicine, Houston, Texas, United States of America.
Abstract:
The pathogenesis of cisplatin-induced acute kidney injury (AKI) is characterized by tubular cell apoptosis and inflammation. However, the molecular mechanisms are not fully understood. We found that CXCL16 was induced in renal tubular epithelial cells in response to cisplatin-induced AKI. Therefore, we investigated whether CXCL16 played a role in cisplatin-induced tubular cell apoptosis and inflammation. Wild-type and CXCL16 knockout mice were administrated with vehicle or cisplatin at 20 mg/kg by intraperitoneal injection. CXCL16 knockout mice had lower blood urea nitrogen and less tubular damage following cisplatin-induced AKI as compared with wild-type mice. Genetic disruption of CXCL16 reduced tubular epithelial cell apoptosis and decreased caspase-3 activation. Furthermore, CXCL16 deficiency inhibited infiltration of macrophages and T cells into the kidneys following cisplatin treatment, which was associated with reduced expression of the proinflammatory cytokines in the kidneys. Taken together, our results indicate that CXCL16 plays a crucial role in the pathogenesis of cisplatin-induced AKI through regulation of apoptosis and inflammation and maybe a novel therapeutic target for cisplatin-induced AKI.
Insights
CXCL16 exacerbates cisplatin-induced acute kidney injury (AKI) by promoting tubular cell apoptosis and inflammation. Targeting CXCL16 may offer a new therapeutic strategy for preventing kidney damage.
Area of Science:
- Nephrology
- Immunology
- Molecular Biology
Background:
- Cisplatin chemotherapy can cause acute kidney injury (AKI), characterized by tubular cell death and inflammation.
- The precise molecular pathways driving cisplatin-induced AKI remain incompletely understood.
- CXCL16 is identified as a molecule upregulated in renal tubular cells during AKI.
Purpose of the Study:
- To investigate the role of CXCL16 in the development of cisplatin-induced AKI.
- To determine if CXCL16 influences tubular cell apoptosis and renal inflammation following cisplatin exposure.
Main Methods:
- Comparison of wild-type and CXCL16 knockout mice treated with cisplatin.
- Assessment of kidney function markers (blood urea nitrogen) and histological damage.
- Evaluation of tubular cell apoptosis, caspase-3 activation, and immune cell infiltration (macrophages, T cells).
- Measurement of pro-inflammatory cytokine expression in kidney tissues.
Main Results:
- CXCL16 knockout mice exhibited reduced blood urea nitrogen and attenuated tubular damage compared to wild-type mice after cisplatin treatment.
- Genetic deletion of CXCL16 significantly decreased tubular epithelial cell apoptosis and caspase-3 activation.
- CXCL16 deficiency led to reduced infiltration of macrophages and T cells into the kidneys.
- Reduced expression of pro-inflammatory cytokines was observed in CXCL16 knockout mice.
Conclusions:
- CXCL16 plays a significant role in the pathogenesis of cisplatin-induced AKI.
- CXCL16 contributes to AKI by promoting tubular cell apoptosis and inflammation.
- CXCL16 represents a potential therapeutic target for mitigating cisplatin-induced kidney damage.
