ArticleToxicological sciences : an official journal of the Society of Toxicology2014
MicroRNA-155 deficient mice experience heightened kidney toxicity when dosed with cisplatin.
Article in Toxicological sciences : an official journal of the Society of Toxicology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 2 of them syntheses that pooled it.
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Who cites it
30 citing papers in PubMed, 2 syntheses or guidelines pooled it, 45 citations in OpenAlex.
- Therapeutic effects of micro-RNAs in preclinical studies of acute kidney injury: a systematic review and meta-analysis.Scientific reports · 2021Pooled it
- Urinary miRNA Biomarkers of Drug-Induced Kidney Injury and Their Site Specificity Within the Nephron.Toxicological sciences : an official journal of the Society of Toxicology · 2021Pooled it
- Review
- A crucial role of miR-155 in the pathomechanism of acute kidney injury.Frontiers in pharmacology · 2025Review
- MicroRNAs in Anticancer Drugs Hepatotoxicity: From Pathogenic Mechanism and Early Diagnosis to Therapeutic Targeting by Natural Products.Current pharmaceutical biotechnology · 2024Review
- Kidney Injury: Focus on Molecular Signaling Pathways.Current medicinal chemistry · 2024Review
- microRNA Expression of Renal Proximal Tubular Epithelial Cells and Their Extracellular Vesicles in an Inflammatory Microenvironment In Vitro.International journal of molecular sciences · 2023Article
- p53 inhibition attenuates cisplatin-induced acute kidney injury through microRNA-142-5p regulating SIRT7/NF-κB.Renal failure · 2022Article
- Istradefylline protects from cisplatin-induced nephrotoxicity and peripheral neuropathy while preserving cisplatin antitumor effects.The Journal of clinical investigation · 2022Article
- MicroRNAs in kidney injury and disease.Nature reviews. Nephrology · 2022Review
- Epigenetic Mechanisms Involved in Cisplatin-Induced Nephrotoxicity: An Update.Pharmaceuticals (Basel, Switzerland) · 2021Review
- The crosstalk between hypoxia-inducible factor-1α and microRNAs in acute kidney injury.Experimental biology and medicine (Maywood, N.J.) · 2020Review
- Emerging role of miRNAs in renal fibrosis.RNA biology · 2020Review
- CircNr1h4 regulates the pathological process of renal injury in salt-sensitive hypertensive mice by targeting miR-155-5p.Journal of cellular and molecular medicine · 2020Article
- miRNA‑mRNA regulatory network analysis of mesenchymal stem cell treatment in cisplatin‑induced acute kidney injury identifies roles for miR‑210/Serpine1 and miR‑378/Fos in regulating inflammation.Molecular medicine reports · 2019Article
- Recent Advances in Models, Mechanisms, Biomarkers, and Interventions in Cisplatin-Induced Acute Kidney Injury.International journal of molecular sciences · 2019Review
- Epigenetic regulation in AKI and kidney repair: mechanisms and therapeutic implications.Nature reviews. Nephrology · 2019Review
- Renal inhibition of miR-181a ameliorates 5-fluorouracil-induced mesangial cell apoptosis and nephrotoxicity.Cell death & disease · 2018Article
- Role of microRNA in the detection, progression, and intervention of acute kidney injury.Experimental biology and medicine (Maywood, N.J.) · 2018Review
- MicroRNAs in injury and repair.Archives of toxicology · 2017Review
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 1 country.
Funding
Abstract
The development of nephrotoxicity limits the maximum achievable dosage and treatment intervals for cisplatin chemotherapy. Therefore, identifying mechanisms that regulate this toxicity could offer novel methods to optimize cisplatin delivery. MicroRNAs are capable of regulating many different genes, and can influence diverse cellular processes, including cell death and apoptosis. We previously observed miR-155 to be highly increased following ischemic or toxic injury to the kidneys and, therefore, sought to determine whether mice deficient in miR-155 would respond differently to kidney injury. We treated C57BL/6 and miR-155(-/-) mice with 20 mg/kg of cisplatin and found a significantly higher level of kidney injury in the miR-155(-/-) mice. Genome-wide expression profiling and bioinformatic analysis indicated the activation of a number of canonical signaling pathways relating to apoptosis and oxidative stress over the course of the injury, and identified potential upstream regulators of these effects. One predicted upstream regulator was c-Fos, which has two confirmed miR-155 binding sites in its 3' UTR and, therefore, can be directly regulated by miR-155. We established that the miR-155(-/-) mice had significantly higher levels of c-Fos mRNA and protein than the C57BL/6 mice at 72 h after cisplatin exposure. These data indicate a role for miR-155 in the cisplatin response and suggest that targeting of c-Fos could be investigated to reduce cisplatin-induced nephrotoxicity.
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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.