Have a personal or library account? Click to login

New Insights in the Pathogenesis of Cisplatin-induced Nephrotoxicity

EABR. Experimental and Applied Biomedical Research
Volume 25 (2024): Issue 3 (September 2024)
By:
Open Access
|Oct 2019

Figures & Tables

Figure 1.

Cisplatin-induced activation of p53 results in apoptosis of tubular cells. Activated p53 increases transcription of pro-apoptotic genes, such as PUMA-α and ER-iPLA2, and down-regulates expression of anti-apoptotic genes (p21 and taurine transporter (TauT)). Additionally, p53 promotes apoptosis of tubular cells through the interactions with Bcl-XL, Bax, Bak proteins in mitochondria and/or cytosol. Abbreviations: Bcl-2: B-cell lymphoma 2; Bcl-xL: B-cell lymphoma-extra large; Bax: Bcl-2-associated X protein; Bak: Bcl-2 homologous antagonist killer; PUMA-α: p53 upregulated modulator of apoptosis; PIDD: p53-induced protein with a death domain; ER-iPLA2: Ca2+-independent phospholipase A2; Cdk2: Cyclin-dependent kinase complex; TauT: taurine transporter.
Cisplatin-induced activation of p53 results in apoptosis of tubular cells. Activated p53 increases transcription of pro-apoptotic genes, such as PUMA-α and ER-iPLA2, and down-regulates expression of anti-apoptotic genes (p21 and taurine transporter (TauT)). Additionally, p53 promotes apoptosis of tubular cells through the interactions with Bcl-XL, Bax, Bak proteins in mitochondria and/or cytosol. Abbreviations: Bcl-2: B-cell lymphoma 2; Bcl-xL: B-cell lymphoma-extra large; Bax: Bcl-2-associated X protein; Bak: Bcl-2 homologous antagonist killer; PUMA-α: p53 upregulated modulator of apoptosis; PIDD: p53-induced protein with a death domain; ER-iPLA2: Ca2+-independent phospholipase A2; Cdk2: Cyclin-dependent kinase complex; TauT: taurine transporter.

Figure 2.

Immunomodulatory molecules which expression is enhanced in renal parenchymal and immune cells upon cisplatin treatment.Cisplatin treatment induces enhanced expression of reactive oxygen species (ROS), inflammatory cytokines and chemokines as well as integrins in the kidneys enabling crosstalk between cisplatin-injured proximal tubular epithelial cells, endothelial cells and renal-infiltrated innate and adaptive immune cells.Abbreviations: ROS: Reactive oxygen species; IL: Interleukin; TNF-α: Tumor necrosis factor alpha; MIF: Macrophage migration inhibitory factor; Mincle: Macrophage-inducible C-type lectin; CXCL1: Chemokine (C-X-C motif) ligand 1; Kim-1: Kidney injury molecule-1; ICAM-1: Intercellular adhesion molecule-1.
Immunomodulatory molecules which expression is enhanced in renal parenchymal and immune cells upon cisplatin treatment.Cisplatin treatment induces enhanced expression of reactive oxygen species (ROS), inflammatory cytokines and chemokines as well as integrins in the kidneys enabling crosstalk between cisplatin-injured proximal tubular epithelial cells, endothelial cells and renal-infiltrated innate and adaptive immune cells.Abbreviations: ROS: Reactive oxygen species; IL: Interleukin; TNF-α: Tumor necrosis factor alpha; MIF: Macrophage migration inhibitory factor; Mincle: Macrophage-inducible C-type lectin; CXCL1: Chemokine (C-X-C motif) ligand 1; Kim-1: Kidney injury molecule-1; ICAM-1: Intercellular adhesion molecule-1.
DOI: https://doi.org/10.2478/sjecr-2019-0012 | Journal eISSN: 2956-2090 | Journal ISSN: 2956-0454
Journal RSS Feed
Language: English
Page range: 275 - 284
Submitted on: Jan 23, 2019
Accepted on: Feb 17, 2019
Published on: Oct 15, 2019
Published by: University of Kragujevac, Faculty of Medical Sciences
In partnership with: Paradigm Publishing Services
Publication frequency: 4 times per year
Keywords:
Cisplatin,
nephrotoxicity,
acute kidney injury,
apoptosis,
inflam-mation
Related subjects:
Medicine,
Clinical medicine,
Clinical medicine, other

© 2019 Bojana Djokovic, Marina Gazdic Jankovic, C. Randall Harrell, Crissy Fellabaum, Nebojsa Arsenijevic, Vladislav Volarevic, published by University of Kragujevac, Faculty of Medical Sciences
This work is licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 License.

Previous articleVolume 25 (2024): Issue 3 (September 2024)Next article