McSweeney Kristen Renee, Gadanec Laura Kate, Qaradakhi Tawar, Ali Benazir Ashiana, Zulli Anthony, Apostolopoulos Vasso
Institute for Health and Sport, Victoria University, Werribee, VIC 3030, Australia.
Cancers (Basel). 2021 Mar 29;13(7):1572. doi: 10.3390/cancers13071572.
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.
化疗药物顺铂的使用会导致急性肾损伤（AKI）。顺铂诱导的急性肾损伤（CIAKI）具有复杂的病理生理过程，这与细胞摄取和外排、细胞凋亡、血管损伤、氧化应激和内质网应激以及炎症反应有关。尽管经过了数十年的研究努力、药物干预和临床试验，但对于接受顺铂治疗的患者，仍没有一种一致且稳定的药物治疗方案来降低急性肾损伤的发生率。这主要是由于对CIAKI病理生理学和相关分子机制的认识不完整。在此，我们详细阐述了顺铂诱导的肾毒性所表现出的广为人知的病理生理学，以及针对这些病理生理过程的各种药理学和基因改变研究。
