ReviewJournal of the American Society of Nephrology : JASN2021
Potential Therapeutic Targets for Cisplatin-Induced Kidney Injury: Lessons from Other Models of AKI and Fibrosis.
Review in Journal of the American Society of Nephrology : JASN, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.
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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
55 citing papers in PubMed, 88 citations in OpenAlex.
- Rosmarinic Acid Alleviates Cisplatin-Induced Acute Kidney Injury by Targeting FYN to Regulate Ferroptosis.Food science & nutrition · 2026Article
- Proanthocyanidins Attenuate Cisplatin-Induced Acute Kidney Injury and are Associated With Reshaping Gut Microbiota and Restoring Redox Homeostasis.Molecular nutrition & food research · 2026Article
- Fluvoxamine and lycopene alleviate cisplatin-induced kidney fibrosis by modulating miR-21 and fibrotic signaling pathways.Scientific reports · 2026Article
- Spirulina and Its Bioactive Compounds as Multi-Target Anticancer Agents: Mechanisms, Immune Modulation, and Translational Potential.Medical sciences (Basel, Switzerland) · 2026Review
- Icaritin Ameliorates Cisplatin-Induced Mitochondrial Metabolic Dysfunction-Associated Nephrotoxicity and Synergistically Potentiates Its Antitumor Efficacy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Phenothiazine alleviates cisplatin-mediated acute kidney injury by inhibiting ferroptosis.Cell and tissue research · 2026Article
- UBE2M Identified by CRISPR Screening as a Key Regulator of Cisplatin-Induced Acute Kidney Injury via the p53 PathwayEndocrine, metabolic & immune disorders drug targets · 2026Article
- NAT10 Promotes Tubular Epithelial Cell Senescence in Cisplatin-Induced Acute Kidney Injury by Regulating DDX17.International journal of biological sciences · 2026Article
- Cisplatin-induced acute kidney injury is alleviated by BMSCs-derived exosome via mmu-miR-874-3p-mediated activation of the wnt/β-catenin signaling pathway.Regenerative therapy · 2025Article
- Assessment of protective effect of the losartan against cisplatin-induced nephrotoxicity in mice.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- Celecoxib has less aggravating effect on cisplatin-induced nephrotoxicity in comparison with non-selective cyclooxygenase inhibitors: a retrospective multi-institutional study.International journal of clinical oncology · 2025Article
- Protective effect of abietic acid nanoparticles synthesized by gamma-irradiation against cisplatin-induced renal injury in mice: a promising novel natural nano-drug.Molecular biology reports · 2025Article
- Intravital imaging of peritubular microcirculation impairment in cisplatin-induced acute kidney injury.JCI insight · 2025Article
- Ultrasound-guided renal subcapsular transplantation of mesenchymal stem cells for treatment of acute kidney injury in a minipig model: safety and efficacy evaluation.Stem cell research & therapy · 2025Article
- Therapeutic role of hucMSC-sEV-enriched miR-13896 in cisplatin-induced acute kidney injury through M2 macrophage polarization.Cell biology and toxicology · 2025Article
- The IDH1-R132H mutation aggravates cisplatin-induced acute kidney injury by promoting ferroptosis through disrupting NDUFA1 and FSP1 interaction.Cell death and differentiation · 2025Article
- A comparative review of murine models of repeated low-dose cisplatin-induced chronic kidney disease.Lab animal · 2025Review
- The spatiotemporal and paradoxical roles of NRF2 in renal toxicity and kidney diseases.Redox biology · 2025Review
- Mitigation of cisplatin-induced acute kidney injury through oral administration of fatty acid amide hydrolase inhibitor PF-04457845.The Journal of pharmacology and experimental therapeutics · 2025Article
- SREBP1c-Mediated Transcriptional Repression of YME1L1 Contributes to Acute Kidney Injury by Inducing Mitochondrial Dysfunction in Tubular Epithelial Cells.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The effectiveness of cisplatin, a mainstay in the treatment of many solid organ cancers, is hindered by dose-limiting nephrotoxicity. Cisplatin causes AKI in 30% of patients. Patients who do not develop AKI by clinical standards during treatment are still at risk for long-term decline in kidney function and the development of CKD. The connection between AKI and CKD has become increasingly studied, with renal fibrosis a hallmark of CKD development. To prevent both the short- and long-term effects of cisplatin, researchers must use models that reflect both types of pathology. Although a lot is known about cisplatin-induced AKI, very little is known about the mechanisms by which repeated low levels of cisplatin lead to fibrosis development. In this review, strategies used in various rodent models to prevent kidney injury, its progression to fibrosis, or both, are examined to gain mechanistic insights and identify potential therapeutic targets for cisplatin-induced kidney pathologies. Reviewing the results from these models highlights the diverse and highly complex role of cell death, cell senescence, endoplasmic reticulum stress, autophagy, and immune cell activation in acute and chronic kidney injuries. The use of several models of kidney injury is needed for development of agents that will prevent all aspects of cisplatin-induced kidney injury.
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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.