Mitochondrial dysregulation and protection in cisplatin nephrotoxicity

Yang, Yuan; Liu, Hong; Liu, Fuyou; Dong, Zheng

doi:10.1007/s00204-014-1239-1

Cited by 128 publications

(91 citation statements)

References 57 publications

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“…Apoptosis of tubular epithelial cells contribute to cisplatin-induced AKI, and inhibition of apoptosis may be therapeutic strategy for cisplatin-induced AKI [25, 26]. In the current study, cisplatin significantly increased the number of TUNEL-positive cells in WT mice, which was markedly reduced by disruption of CXCL16.…”

Section: Discussionmentioning

confidence: 52%

CXCL16 regulates cisplatin-induced acute kidney injury

Liu

Zhang

et al. 2016

Oncotarget

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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.

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Section: Discussionmentioning

confidence: 52%

CXCL16 regulates cisplatin-induced acute kidney injury

Liu

Zhang

et al. 2016

Oncotarget

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“…However, accumulating evidence suggests that DNA damage and the associated DNA damage response (DDR) are the indispensable pathogenic mechanism. p53, a well-known tumor suppressor protein, is considered closely related to DNA damage induced by cisplatin [16]. In 2010, we reported the first evidence of microRNA regulation in cisplatin nephrotoxicity [17].…”

Section: Microrna In Cisplatin Nephrotoxic Akimentioning

confidence: 99%

MicroRNAs in Pathogenesis of Acute Kidney Injury

Liu

Wang²,

et al. 2016

Nephron

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MicroRNAs (miRNAs) are small non-coding RNAs that regulate gene expression mainly by repressing their target gene translation. A large spectrum of human diseases is associated with significant changes in miRNAs. Many miRNAs are induced in diseases, whereas some others are downregulated. The significance of miRNAs has been demonstrated in renal development and physiology, and in major kidney diseases such as acute kidney injury (AKI). Recent studies have further implicated specific miRNAs in the pathogenesis of AKI. miRNAs also have the potential to become new diagnostic biomarkers of AKI. Further investigation will identify the key pathogenic miRNAs in various types of AKI and test miRNA-based therapeutics and diagnosis.

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“…HK-2 cells were treated with SSD (0,20,40,60,80,100 or 150 μM) for 24 h (A) and were then uniformly treated with the maximum dose of SSD (100 μM) for different periods (0, 6, 12, 24 or 48 h; B). The cells were treated with DDP (0, 2.5, 5, 10, 20 or 30 μM) for 24 h (C) and were pretreated with SSD (100 μM) for different periods (0, 15 min, 30 min, 1 h, 2 h, 4 h, 8 h, 16 h or 32 h) and were pretreated with SSD (20,40,60,80,100 or 150 μM) for 2 h and then were treated with 10 μM DDP (E) for 24 h. Cell viability was determined using the CCK-8 assay according to the absorbance value (A). The data are presented as the mean values ± SD from five independent experiments.…”

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confidence: 99%