Recent Advances in Models, Mechanisms, Biomarkers, and Interventions in Cisplatin-Induced Acute Kidney Injury

Holditch, Sara J.; Brown, Carolyn N.; Lombardi, Andrew M.; Nguyen, Khoa N.; Edelstein, Charles L.

doi:10.3390/ijms20123011

Submit to this Journal Review for this Journal Edit a Special Issue

Article Menu

...

Open AccessReview

Recent Advances in Models, Mechanisms, Biomarkers, and Interventions in Cisplatin-Induced Acute Kidney Injury

and

Division of Renal Diseases and Hypertension, University of Colorado at Denver, Box C281, 12700 East, 19th Ave, Aurora, CO 80045, USA

Author to whom correspondence should be addressed.

Int. J. Mol. Sci. 2019, 20(12), 3011; https://doi.org/10.3390/ijms20123011

Received: 10 May 2019 / Revised: 31 May 2019 / Accepted: 12 June 2019 / Published: 20 June 2019

(This article belongs to the Special Issue Cisplatin in Cancer Therapy: Molecular Mechanisms of Action)

View Full-Text Download PDF

Browse Figure

Review Reports Citation Export

Abstract

Cisplatin is a widely used chemotherapeutic agent used to treat solid tumours, such as ovarian, head and neck, and testicular germ cell. A known complication of cisplatin administration is acute kidney injury (AKI). The development of effective tumour interventions with reduced nephrotoxicity relies heavily on understanding the molecular pathophysiology of cisplatin-induced AKI. Rodent models have provided mechanistic insight into the pathophysiology of cisplatin-induced AKI. In the subsequent review, we provide a detailed discussion of recent advances in the cisplatin-induced AKI phenotype, principal mechanistic findings of injury and therapy, and pre-clinical use of AKI rodent models. Cisplatin-induced AKI murine models faithfully develop gross manifestations of clinical AKI such as decreased kidney function, increased expression of tubular injury biomarkers, and tubular injury evident by histology. Pathways involved in AKI include apoptosis, necrosis, inflammation, and increased oxidative stress, ultimately providing a translational platform for testing the therapeutic efficacy of potential interventions. This review provides a discussion of the foundation laid by cisplatin-induced AKI rodent models for our current understanding of AKI molecular pathophysiology. View Full-Text

Keywords: cisplatin; acute kidney injury; AKI; apoptosis; inflammation; oxidative stress

▼ Show Figures

Figure 1

This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited

Share and Cite

MDPI and ACS Style

Holditch, S.J.; Brown, C.N.; Lombardi, A.M.; Nguyen, K.N.; Edelstein, C.L. Recent Advances in Models, Mechanisms, Biomarkers, and Interventions in Cisplatin-Induced Acute Kidney Injury. Int. J. Mol. Sci. 2019, 20, 3011. https://doi.org/10.3390/ijms20123011

AMA Style

Holditch SJ, Brown CN, Lombardi AM, Nguyen KN, Edelstein CL. Recent Advances in Models, Mechanisms, Biomarkers, and Interventions in Cisplatin-Induced Acute Kidney Injury. International Journal of Molecular Sciences. 2019; 20(12):3011. https://doi.org/10.3390/ijms20123011

Chicago/Turabian Style

Holditch, Sara J., Carolyn N. Brown, Andrew M. Lombardi, Khoa N. Nguyen, and Charles L. Edelstein. 2019. "Recent Advances in Models, Mechanisms, Biomarkers, and Interventions in Cisplatin-Induced Acute Kidney Injury" International Journal of Molecular Sciences 20, no. 12: 3011. https://doi.org/10.3390/ijms20123011

Find Other Styles

Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.

Article Metrics

Abstract views Pdf views Html views

Article Menu

Recent Advances in Models, Mechanisms, Biomarkers, and Interventions in Cisplatin-Induced Acute Kidney Injury

Abstract

Share and Cite

Article Metrics

Article Access Statistics

Article Access Map by Country/Region

Further Information

Guidelines

MDPI Initiatives

Follow MDPI