Mechanisms of Cisplatin-Induced Acute Kidney Injury: Pathological Mechanisms, Pharmacological Interventions, and Genetic Mitigations.
AKI
acute kidney injury
cisplatin
cisplatin-induced acute kidney injury
nephrotoxicity
Journal
Cancers
ISSN: 2072-6694
Titre abrégé: Cancers (Basel)
Pays: Switzerland
ID NLM: 101526829
Informations de publication
Date de publication:
29 Mar 2021
29 Mar 2021
Historique:
received:
29
01
2021
revised:
19
03
2021
accepted:
25
03
2021
entrez:
3
4
2021
pubmed:
4
4
2021
medline:
4
4
2021
Statut:
epublish
Résumé
Administration of the chemotherapeutic agent cisplatin leads to acute kidney injury (AKI). Cisplatin-induced AKI (CIAKI) has a complex pathophysiological map, which has been linked to cellular uptake and efflux, apoptosis, vascular injury, oxidative and endoplasmic reticulum stress, and inflammation. Despite research efforts, pharmaceutical interventions, and clinical trials spanning over several decades, a consistent and stable pharmacological treatment option to reduce AKI in patients receiving cisplatin remains unavailable. This has been predominately linked to the incomplete understanding of CIAKI pathophysiology and molecular mechanisms involved. Herein, we detail the extensively known pathophysiology of cisplatin-induced nephrotoxicity that manifests and the variety of pharmacological and genetic alteration studies that target them.
Identifiants
pubmed: 33805488
pii: cancers13071572
doi: 10.3390/cancers13071572
pmc: PMC8036620
pii:
doi:
Types de publication
Journal Article
Review
Langues
eng
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