Abstract
Mitochondrial transplantation (MT) is a new experimental approach that has demonstrated positive results reverting mitochondrial alterations in cardiac and kidney dysfunction mainly mediated by oxidative stress. On the other hand, cisplatin is an effective and widely used antineoplastic drug in treating several cancers; however, cisplatin has notorious side effects in different organs, such as the heart, kidneys, liver, and brain; the kidney being one of the most affected. The genitourinary system is the principal excretion pathway of cisplatin, since it is removed from the blood primarily by glomerular filtration and tubular secretion, and it may cause a sudden reduction in the renal function (acute kidney injury “AKI”), in part, by inducing mitochondrial dysfunction and the consequent oxidative stress in the tubular segment. In addition, AKI may associate with cardiac alterations, as occurs in acute cardiorenal syndrome. Due to the high prevalence of renal and cardiac side effects produced by cisplatin, here we discuss the possible use of MT as a novel therapy that could protect tissues by alleviating mitochondrial dysfunction and reducing reactive oxygen species (ROS) production.
Highlights
Mitochondrial transplantation (MT) is a new experimental approach that has demonstrated positive results reverting mitochondrial alterations in cardiac and kidney dysfunction mainly mediated by oxidative stress
Cisplatin enters into the tubular cells by passive diffusion or by cellular transporters, such as copper enters into the tubular cells by passive diffusion or by cellular transporters, such as copper transport protein 1 (Ctr1); the basolateral organic cation transporter 2 (OCT-2), which is highly expressed in renal tubular cells [25,47]; and the less explored volume regulated anion channels (VRAC) [26]
It is interesting to mention that this study evaluated the comparison between N-acetylcysteine and the MT, observing that N-acetylcysteine provided partial improvement compared to MT, which suggests that exogenous mitochondria could be a more effective therapy in treating drug induced liver toxicity
Summary
Acute kidney injury (AKI) is a clinical syndrome, defined by an abrupt decrease in glomerular filtration, that encompasses several clinical scenarios, aetiologies, comorbidities, drug exposures and severities of renal dysfunction [1,2]. Drugs are the third to the fifth leading cause of AKI in the intensive care unit [3,4]. Drug induced AKI accounts for 20–30% of critically ill patients [3] and may play a causative role in as many as. 20% of the cases require renal replacement therapy [3], which is related to increased mortality, and this reaches rates of over 60% in developing countries [7]. Acute tubular necrosis is the most common intrinsic kidney injury, mainly caused by the basolateral and apical efflux of several drugs, Future Pharm. Future Pharm. 2021, 1 such as antimicrobials, antivirals, chemotherapeutics, immunosuppressants, radiocontrast agents and others [8,9]
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