ArticlePloS one2015
Mechanism of Cisplatin-Induced Cytotoxicity Is Correlated to Impaired Metabolism Due to Mitochondrial ROS Generation.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 150 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
150 citing papers in PubMed, 1 synthesis or guideline pooled it, 277 citations in OpenAlex.
- Pooled it
- Trial
- An HRedox biology · 2026Article
- Chemotherapeutic Potential of Fluorouracil-Platinum (IV) Prodrugs Against Cisplatin-Resistant Colorectal Cancer Cells.Chemistry (Weinheim an der Bergstrasse, Germany) · 2026Article
- Exercise attenuates cisplatin-induced anorexia-cachexia via modulation of hypothalamic inflammation and orexigenic signaling.European journal of applied physiology · 2026Article
- Synergistic Effect of Digoxin and Cisplatin on Redox Imbalance in HeLa Cells.Cell biochemistry and function · 2026Article
- Ambrisentan attenuates cisplatin-related mitochondrial dysfunction in the heart via regulation of p53 and NF-κB signaling.Scientific reports · 2026Article
- Morin hydrate alleviated cisplatin-induced testicular toxicity in rats via modulating NLRP3/NF-κB pathway.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Protective effect of trans-sodium crocetinate on nephrotoxicity induced by cisplatin: in vitro and in vivo models.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- An AOP-guidedNAM journal · 2026Article
- GCN2 in Cancer: Molecular Mechanisms to Therapeutic Potential.Current cancer drug targets · 2026Review
- Identification of diagnostic biomarkers and mitochondrial metabolic characteristics in sepsis-associated acute kidney injury.European journal of medical research · 2025Article
- Cisplatin-induced genetic alterations in KEAP1 promote therapeutic resistance in head and neck squamous cell carcinoma.Redox biology · 2025Article
- Comparative Antioxidant Protection of Cochlear Hair Cells from Ototoxins.Molecules (Basel, Switzerland) · 2025Article
- Article
- Potential beneficial effects of dietary replacement of fish meal with Black soldier fly (Hermetia illucens) larvae meal on growth, general physiology, and microanatomy of Nile tilapia (Oreochromis niloticus).Fish physiology and biochemistry · 2025Article
- Evaluation of the impact ofHistology and histopathology · 2025Article
- Antitumor Activity of Isalpinin fromMolecules (Basel, Switzerland) · 2025Article
- Nano Spirulina platensis countered cisplatin-induced repro-toxicity by reversing the expression of altered steroid hormones and downregulation of the StAR gene.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- Article
90 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The chemotherapeutic use of cisplatin is limited by its severe side effects. In this study, by conducting different omics data analyses, we demonstrated that cisplatin induces cell death in a proximal tubular cell line by suppressing glycolysis- and tricarboxylic acid (TCA)/mitochondria-related genes. Furthermore, analysis of the urine from cisplatin-treated rats revealed the lower expression levels of enzymes involved in glycolysis, TCA cycle, and genes related to mitochondrial stability and confirmed the cisplatin-related metabolic abnormalities. Additionally, an increase in the level of p53, which directly inhibits glycolysis, has been observed. Inhibition of p53 restored glycolysis and significantly reduced the rate of cell death at 24 h and 48 h due to p53 inhibition. The foremost reason of cisplatin-related cytotoxicity has been correlated to the generation of mitochondrial reactive oxygen species (ROS) that influence multiple pathways. Abnormalities in these pathways resulted in the collapse of mitochondrial energy production, which in turn sensitized the cells to death. The quenching of ROS led to the amelioration of the affected pathways. Considering these observations, it can be concluded that there is a significant correlation between cisplatin and metabolic dysfunctions involving mROS as the major player.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.