Mechanisms of Cisplatin-Induced Acute Kidney Injury: Pathological Mechanisms, Pharmacological Interventions, and Genetic Mitigations.
Mechanisms of Cisplatin-Induced Acute Kidney Injury: Pathological Mechanisms, Pharmacological Interventions, and Genetic Mitigations.
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DOI：
10.3390/cancers13071572
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发表时间：
2021-03-29
期刊：
影响因子：
5.2
通讯作者：
Apostolopoulos V
中科院分区：
文献类型：
--
作者：
McSweeney KR;Gadanec LK;Qaradakhi T;Ali BA;Zulli A;Apostolopoulos V
肾毒性是顺铂治疗的剂量限制因素。肾毒性的特征是肾功能下降。虽然这种情况往往是可逆的，但在顺铂停止治疗数年后，效果显著。它有一个广泛的病理生理学图谱。这篇文章的目的是巩固顺铂所致急性肾损伤的文献，并将其集中在一篇论文中。它探索了与这种疾病有关的每一种个体机制，已经测试过的针对每一种疾病的药理学选择，以及每项研究获得的结果。文章还介绍了基因改造研究及其在预防疾病发展方面的有效性。化疗药物顺铂会导致急性肾损伤(AKI)。顺铂诱导的AKI(CIAKI)有一个复杂的病理生理图谱，与细胞摄取和外排、细胞凋亡、血管损伤、氧化和内质网应激以及炎症有关。尽管经过几十年的研究努力、药物干预和临床试验，但仍没有一致和稳定的药物治疗方案来减少接受顺铂治疗的患者的AKI。这主要与对CIAKI的病理生理学和分子机制的不完全了解有关。在这里，我们详细介绍了广泛已知的顺铂肾毒性的病理生理学表现，以及针对它们的各种药理和遗传改变研究。
Nephrotoxicity is the dose-limiting factor of cisplatin treatment. Nephrotoxicity is characterized by reduced kidney function. Although an often-reversible condition, effects are notably seen years after treatment with cisplatin has ceased. It has an extensive pathophysiological map. The purpose of this article is to consolidate cisplatin-induced acute kidney injury literature and present it in one collective paper. It explores each individual mechanism linked to the disease, the pharmacological options that have been tested to target each of them, and the results obtained by each study. The paper also describes genetic modification studies and their effectiveness in preventing disease development. 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.
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